---
_id: '51'
abstract:
- lang: eng
text: Asymmetries have long been known about in the central nervous system. From
gross anatomical differences, such as the presence of the parapineal organ in
only one hemisphere of the developing zebrafish, to more subtle differences in
activity between both hemispheres, as seen in freely roaming animals or human
participants under PET and fMRI imaging analysis. The presence of asymmetries
has been demonstrated to have huge behavioural implications, with their disruption
often leading to the generation of neurological disorders, memory problems, changes
in personality, and in an organism's health and well-being. For my Ph.D. work
I aimed to tackle two important avenues of research. The first being the process
of input-side dependency in the hippocampus, with the goal of finding a key gene
responsible for its development (Gene X). The second project was to do with experience-induced
laterality formation in the hippocampus. Specifically, how laterality in the synapse
density of the CA1 stratum radiatum (s.r.) could be induced purely through environmental
enrichment. Through unilateral tracer injections into the CA3, I was able to selectively
measure the properties of synapses within the CA1 and investigate how they differed
based upon which hemisphere the presynaptic neurone originated. Having found the
existence of a previously unreported reversed (left-isomerism) i.v. mutant, through
morpholocal examination of labelled terminals in the CA1 s.r., I aimed to elucidate
a key gene responsible for the process of left or right determination of inputs
to the CA1 s.r.. This work relates to the previous finding of input-side dependent
asymmetry in the wild-type rodent, where the origin of the projecting neurone
to the CA1 will determine the morphology of a synapse, to a greater degree than
the hemisphere in which the projection terminates. Using left- and right-isomerism
i.v. mice, in combination with whole genome sequence analysis, I highlight Ena/VASP-like
(Evl) as a potential target for Gene X. In relation to this topic, I also highlight
my work in the recently published paper of how knockout of PirB can lead to a
lack of input-side dependency in the murine hippocampus. For the second question,
I show that the environmental enrichment paradigm will lead to an asymmetry in
the synapse densities in the hippocampus of mice. I also highlight that the nature
of the enrichment is of less consequence than the process of enrichment itself.
I demonstrate that the CA3 region will dramatically alter its projection targets,
in relation to environmental stimulation, with the asymmetry in synaptic density,
caused by enrichment, relying heavily on commissural fibres. I also highlight
the vital importance of input-side dependent asymmetry, as a necessary component
of experience-dependent laterality formation in the CA1 s.r.. However, my results
suggest that it isn't the only cause, as there appears to be a CA1 dependent mechanism
also at play. Upon further investigation, I highlight the significant, and highly
important, finding that the changes seen in the CA1 s.r. were predominantly caused
through projections from the left-CA3, with the right-CA3 having less involvement
in this mechanism.
alternative_title:
- ISTA Thesis
article_processing_charge: No
author:
- first_name: Matthew J
full_name: Case, Matthew J
id: 44B7CA5A-F248-11E8-B48F-1D18A9856A87
last_name: Case
citation:
ama: 'Case MJ. From the left to the right: A tale of asymmetries, environments,
and hippocampal development. 2018. doi:10.15479/AT:ISTA:th_1032'
apa: 'Case, M. J. (2018). From the left to the right: A tale of asymmetries,
environments, and hippocampal development. Institute of Science and Technology
Austria. https://doi.org/10.15479/AT:ISTA:th_1032'
chicago: 'Case, Matthew J. “From the Left to the Right: A Tale of Asymmetries, Environments,
and Hippocampal Development.” Institute of Science and Technology Austria, 2018.
https://doi.org/10.15479/AT:ISTA:th_1032.'
ieee: 'M. J. Case, “From the left to the right: A tale of asymmetries, environments,
and hippocampal development,” Institute of Science and Technology Austria, 2018.'
ista: 'Case MJ. 2018. From the left to the right: A tale of asymmetries, environments,
and hippocampal development. Institute of Science and Technology Austria.'
mla: 'Case, Matthew J. From the Left to the Right: A Tale of Asymmetries, Environments,
and Hippocampal Development. Institute of Science and Technology Austria,
2018, doi:10.15479/AT:ISTA:th_1032.'
short: 'M.J. Case, From the Left to the Right: A Tale of Asymmetries, Environments,
and Hippocampal Development, Institute of Science and Technology Austria, 2018.'
date_created: 2018-12-11T11:44:22Z
date_published: 2018-06-27T00:00:00Z
date_updated: 2023-09-07T12:39:22Z
day: '27'
ddc:
- '571'
- '576'
degree_awarded: PhD
department:
- _id: RySh
doi: 10.15479/AT:ISTA:th_1032
file:
- access_level: closed
checksum: dcc7b55619d8509dd62b8e99d6cdee44
content_type: application/msword
creator: dernst
date_created: 2019-04-09T07:16:26Z
date_updated: 2021-02-11T23:30:13Z
embargo_to: open_access
file_id: '6251'
file_name: 2018_Thesis_Case_Source.doc
file_size: 141270528
relation: source_file
- access_level: open_access
checksum: f69fdd5c8709c4e618aa8c1a1221153d
content_type: application/pdf
creator: dernst
date_created: 2019-04-09T07:16:23Z
date_updated: 2021-02-11T11:17:14Z
embargo: 2019-07-05
file_id: '6252'
file_name: 2018_Thesis_Case.pdf
file_size: 15193621
relation: main_file
file_date_updated: 2021-02-11T23:30:13Z
has_accepted_license: '1'
language:
- iso: eng
month: '06'
oa: 1
oa_version: Published Version
page: '186'
publication_identifier:
issn:
- 2663-337X
publication_status: published
publisher: Institute of Science and Technology Austria
publist_id: '8003'
pubrep_id: '1032'
related_material:
record:
- id: '682'
relation: part_of_dissertation
status: public
status: public
supervisor:
- first_name: Ryuichi
full_name: Shigemoto, Ryuichi
id: 499F3ABC-F248-11E8-B48F-1D18A9856A87
last_name: Shigemoto
orcid: 0000-0001-8761-9444
title: 'From the left to the right: A tale of asymmetries, environments, and hippocampal
development'
type: dissertation
user_id: c635000d-4b10-11ee-a964-aac5a93f6ac1
year: '2018'
...
---
_id: '562'
abstract:
- lang: eng
text: Primary neuronal cell culture preparations are widely used to investigate
synaptic functions. This chapter describes a detailed protocol for the preparation
of a neuronal cell culture in which giant calyx-type synaptic terminals are formed.
This chapter also presents detailed protocols for utilizing the main technical
advantages provided by such a preparation, namely, labeling and imaging of synaptic
organelles and electrophysiological recordings directly from presynaptic terminals.
alternative_title:
- Methods in Molecular Biology
article_processing_charge: No
author:
- first_name: Dimitar
full_name: Dimitrov, Dimitar
last_name: Dimitrov
- first_name: Laurent
full_name: Guillaud, Laurent
last_name: Guillaud
- first_name: Kohgaku
full_name: Eguchi, Kohgaku
id: 2B7846DC-F248-11E8-B48F-1D18A9856A87
last_name: Eguchi
orcid: 0000-0002-6170-2546
- first_name: Tomoyuki
full_name: Takahashi, Tomoyuki
last_name: Takahashi
citation:
ama: 'Dimitrov D, Guillaud L, Eguchi K, Takahashi T. Culture of mouse giant central
nervous system synapses and application for imaging and electrophysiological analyses.
In: Skaper SD, ed. Neurotrophic Factors. Vol 1727. Springer; 2018:201-215.
doi:10.1007/978-1-4939-7571-6_15'
apa: Dimitrov, D., Guillaud, L., Eguchi, K., & Takahashi, T. (2018). Culture
of mouse giant central nervous system synapses and application for imaging and
electrophysiological analyses. In S. D. Skaper (Ed.), Neurotrophic Factors
(Vol. 1727, pp. 201–215). Springer. https://doi.org/10.1007/978-1-4939-7571-6_15
chicago: Dimitrov, Dimitar, Laurent Guillaud, Kohgaku Eguchi, and Tomoyuki Takahashi.
“Culture of Mouse Giant Central Nervous System Synapses and Application for Imaging
and Electrophysiological Analyses.” In Neurotrophic Factors, edited by
Stephen D. Skaper, 1727:201–15. Springer, 2018. https://doi.org/10.1007/978-1-4939-7571-6_15.
ieee: D. Dimitrov, L. Guillaud, K. Eguchi, and T. Takahashi, “Culture of mouse giant
central nervous system synapses and application for imaging and electrophysiological
analyses,” in Neurotrophic Factors, vol. 1727, S. D. Skaper, Ed. Springer,
2018, pp. 201–215.
ista: 'Dimitrov D, Guillaud L, Eguchi K, Takahashi T. 2018.Culture of mouse giant
central nervous system synapses and application for imaging and electrophysiological
analyses. In: Neurotrophic Factors. Methods in Molecular Biology, vol. 1727, 201–215.'
mla: Dimitrov, Dimitar, et al. “Culture of Mouse Giant Central Nervous System Synapses
and Application for Imaging and Electrophysiological Analyses.” Neurotrophic
Factors, edited by Stephen D. Skaper, vol. 1727, Springer, 2018, pp. 201–15,
doi:10.1007/978-1-4939-7571-6_15.
short: D. Dimitrov, L. Guillaud, K. Eguchi, T. Takahashi, in:, S.D. Skaper (Ed.),
Neurotrophic Factors, Springer, 2018, pp. 201–215.
date_created: 2018-12-11T11:47:11Z
date_published: 2018-01-01T00:00:00Z
date_updated: 2021-01-12T08:03:05Z
day: '01'
ddc:
- '570'
department:
- _id: RySh
doi: 10.1007/978-1-4939-7571-6_15
editor:
- first_name: Stephen D.
full_name: Skaper, Stephen D.
last_name: Skaper
external_id:
pmid:
- '29222783'
file:
- access_level: open_access
checksum: 8aa174ca65a56fbb19e9f88cff3ac3fd
content_type: application/pdf
creator: dernst
date_created: 2019-11-19T07:47:43Z
date_updated: 2020-07-14T12:47:09Z
file_id: '7046'
file_name: 2018_NeurotrophicFactors_Dimitrov.pdf
file_size: 787407
relation: main_file
file_date_updated: 2020-07-14T12:47:09Z
has_accepted_license: '1'
intvolume: ' 1727'
language:
- iso: eng
month: '01'
oa: 1
oa_version: Submitted Version
page: 201 - 215
pmid: 1
publication: Neurotrophic Factors
publication_status: published
publisher: Springer
publist_id: '7252'
quality_controlled: '1'
scopus_import: 1
status: public
title: Culture of mouse giant central nervous system synapses and application for
imaging and electrophysiological analyses
type: book_chapter
user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87
volume: 1727
year: '2018'
...
---
_id: '612'
abstract:
- lang: eng
text: Metabotropic GABAB receptors mediate slow inhibitory effects presynaptically
and postsynaptically through the modulation of different effector signalling pathways.
Here, we analysed the distribution of GABAB receptors using highly sensitive SDS-digested
freeze-fracture replica labelling in mouse cerebellar Purkinje cells. Immunoreactivity
for GABAB1 was observed on presynaptic and, more abundantly, on postsynaptic compartments,
showing both scattered and clustered distribution patterns. Quantitative analysis
of immunoparticles revealed a somato-dendritic gradient, with the density of immunoparticles
increasing 26-fold from somata to dendritic spines. To understand the spatial
relationship of GABAB receptors with two key effector ion channels, the G protein-gated
inwardly rectifying K+ (GIRK/Kir3) channel and the voltage-dependent Ca2+ channel,
biochemical and immunohistochemical approaches were performed. Co-immunoprecipitation
analysis demonstrated that GABAB receptors co-assembled with GIRK and CaV2.1 channels
in the cerebellum. Using double-labelling immunoelectron microscopic techniques,
co-clustering between GABAB1 and GIRK2 was detected in dendritic spines, whereas
they were mainly segregated in the dendritic shafts. In contrast, co-clustering
of GABAB1 and CaV2.1 was detected in dendritic shafts but not spines. Presynaptically,
although no significant co-clustering of GABAB1 and GIRK2 or CaV2.1 channels was
detected, inter-cluster distance for GABAB1 and GIRK2 was significantly smaller
in the active zone than in the dendritic shafts, and that for GABAB1 and CaV2.1
was significantly smaller in the active zone than in the dendritic shafts and
spines. Thus, GABAB receptors are associated with GIRK and CaV2.1 channels in
different subcellular compartments. These data provide a better framework for
understanding the different roles played by GABAB receptors and their effector
ion channels in the cerebellar network.
article_processing_charge: No
article_type: original
author:
- first_name: Rafael
full_name: Luján, Rafael
last_name: Luján
- first_name: Carolina
full_name: Aguado, Carolina
last_name: Aguado
- first_name: Francisco
full_name: Ciruela, Francisco
last_name: Ciruela
- first_name: Javier
full_name: Cózar, Javier
last_name: Cózar
- first_name: David
full_name: Kleindienst, David
id: 42E121A4-F248-11E8-B48F-1D18A9856A87
last_name: Kleindienst
- first_name: Luis
full_name: De La Ossa, Luis
last_name: De La Ossa
- first_name: Bernhard
full_name: Bettler, Bernhard
last_name: Bettler
- first_name: Kevin
full_name: Wickman, Kevin
last_name: Wickman
- first_name: Masahiko
full_name: Watanabe, Masahiko
last_name: Watanabe
- first_name: Ryuichi
full_name: Shigemoto, Ryuichi
id: 499F3ABC-F248-11E8-B48F-1D18A9856A87
last_name: Shigemoto
orcid: 0000-0001-8761-9444
- first_name: Yugo
full_name: Fukazawa, Yugo
last_name: Fukazawa
citation:
ama: Luján R, Aguado C, Ciruela F, et al. Differential association of GABAB receptors
with their effector ion channels in Purkinje cells. Brain Structure and Function.
2018;223(3):1565-1587. doi:10.1007/s00429-017-1568-y
apa: Luján, R., Aguado, C., Ciruela, F., Cózar, J., Kleindienst, D., De La Ossa,
L., … Fukazawa, Y. (2018). Differential association of GABAB receptors with their
effector ion channels in Purkinje cells. Brain Structure and Function.
Springer. https://doi.org/10.1007/s00429-017-1568-y
chicago: Luján, Rafael, Carolina Aguado, Francisco Ciruela, Javier Cózar, David
Kleindienst, Luis De La Ossa, Bernhard Bettler, et al. “Differential Association
of GABAB Receptors with Their Effector Ion Channels in Purkinje Cells.” Brain
Structure and Function. Springer, 2018. https://doi.org/10.1007/s00429-017-1568-y.
ieee: R. Luján et al., “Differential association of GABAB receptors with
their effector ion channels in Purkinje cells,” Brain Structure and Function,
vol. 223, no. 3. Springer, pp. 1565–1587, 2018.
ista: Luján R, Aguado C, Ciruela F, Cózar J, Kleindienst D, De La Ossa L, Bettler
B, Wickman K, Watanabe M, Shigemoto R, Fukazawa Y. 2018. Differential association
of GABAB receptors with their effector ion channels in Purkinje cells. Brain Structure
and Function. 223(3), 1565–1587.
mla: Luján, Rafael, et al. “Differential Association of GABAB Receptors with Their
Effector Ion Channels in Purkinje Cells.” Brain Structure and Function,
vol. 223, no. 3, Springer, 2018, pp. 1565–87, doi:10.1007/s00429-017-1568-y.
short: R. Luján, C. Aguado, F. Ciruela, J. Cózar, D. Kleindienst, L. De La Ossa,
B. Bettler, K. Wickman, M. Watanabe, R. Shigemoto, Y. Fukazawa, Brain Structure
and Function 223 (2018) 1565–1587.
date_created: 2018-12-11T11:47:29Z
date_published: 2018-04-01T00:00:00Z
date_updated: 2024-03-25T23:30:16Z
day: '01'
ddc:
- '571'
department:
- _id: RySh
doi: 10.1007/s00429-017-1568-y
ec_funded: 1
external_id:
isi:
- '000428419500030'
file:
- access_level: open_access
checksum: a55b3103476ecb5f4f983d8801807e8b
content_type: application/pdf
creator: system
date_created: 2018-12-12T10:15:36Z
date_updated: 2020-07-14T12:47:20Z
file_id: '5157'
file_name: IST-2018-1013-v1+1_2018_Kleindienst_Differential.pdf
file_size: 5542926
relation: main_file
file_date_updated: 2020-07-14T12:47:20Z
has_accepted_license: '1'
intvolume: ' 223'
isi: 1
issue: '3'
language:
- iso: eng
month: '04'
oa: 1
oa_version: Published Version
page: 1565 - 1587
project:
- _id: 25CBA828-B435-11E9-9278-68D0E5697425
call_identifier: H2020
grant_number: '720270'
name: Human Brain Project Specific Grant Agreement 1 (HBP SGA 1)
- _id: 25681D80-B435-11E9-9278-68D0E5697425
call_identifier: FP7
grant_number: '291734'
name: International IST Postdoc Fellowship Programme
publication: Brain Structure and Function
publication_status: published
publisher: Springer
publist_id: '7192'
pubrep_id: '1013'
quality_controlled: '1'
related_material:
record:
- id: '9562'
relation: dissertation_contains
status: public
scopus_import: '1'
status: public
title: Differential association of GABAB receptors with their effector ion channels
in Purkinje cells
tmp:
image: /images/cc_by.png
legal_code_url: https://creativecommons.org/licenses/by/4.0/legalcode
name: Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)
short: CC BY (4.0)
type: journal_article
user_id: c635000d-4b10-11ee-a964-aac5a93f6ac1
volume: 223
year: '2018'
...
---
_id: '41'
abstract:
- lang: eng
text: 'The small-conductance, Ca2+-activated K+ (SK) channel subtype SK2 regulates
the spike rate and firing frequency, as well as Ca2+ transients in Purkinje cells
(PCs). To understand the molecular basis by which SK2 channels mediate these functions,
we analyzed the exact location and densities of SK2 channels along the neuronal
surface of the mouse cerebellar PCs using SDS-digested freeze-fracture replica
labeling (SDS-FRL) of high sensitivity combined with quantitative analyses. Immunogold
particles for SK2 were observed on post- and pre-synaptic compartments showing
both scattered and clustered distribution patterns. We found an axo-somato-dendritic
gradient of the SK2 particle density increasing 12-fold from soma to dendritic
spines. Using two different immunogold approaches, we also found that SK2 immunoparticles
were frequently adjacent to, but never overlap with, the postsynaptic density
of excitatory synapses in PC spines. Co-immunoprecipitation analysis demonstrated
that SK2 channels form macromolecular complexes with two types of proteins that
mobilize Ca2+: CaV2.1 channels and mGlu1α receptors in the cerebellum. Freeze-fracture
replica double-labeling showed significant co-clustering of particles for SK2
with those for CaV2.1 channels and mGlu1α receptors. SK2 channels were also detected
at presynaptic sites, mostly at the presynaptic active zone (AZ), where they are
close to CaV2.1 channels, though they are not significantly co-clustered. These
data demonstrate that SK2 channels located in different neuronal compartments
can associate with distinct proteins mobilizing Ca2+, and suggest that the ultrastructural
association of SK2 with CaV2.1 and mGlu1α provides the mechanism that ensures
voltage (excitability) regulation by distinct intracellular Ca2+ transients in
PCs.'
article_number: '311'
article_processing_charge: No
article_type: original
author:
- first_name: Rafæl
full_name: Luján, Rafæl
last_name: Luján
- first_name: Carolina
full_name: Aguado, Carolina
last_name: Aguado
- first_name: Francisco
full_name: Ciruela, Francisco
last_name: Ciruela
- first_name: Xavier
full_name: Arus, Xavier
last_name: Arus
- first_name: Alejandro
full_name: Martín Belmonte, Alejandro
last_name: Martín Belmonte
- first_name: Rocío
full_name: Alfaro Ruiz, Rocío
last_name: Alfaro Ruiz
- first_name: Jesus
full_name: Martinez Gomez, Jesus
last_name: Martinez Gomez
- first_name: Luis
full_name: De La Ossa, Luis
last_name: De La Ossa
- first_name: Masahiko
full_name: Watanabe, Masahiko
last_name: Watanabe
- first_name: John
full_name: Adelman, John
last_name: Adelman
- first_name: Ryuichi
full_name: Shigemoto, Ryuichi
id: 499F3ABC-F248-11E8-B48F-1D18A9856A87
last_name: Shigemoto
orcid: 0000-0001-8761-9444
- first_name: Yugo
full_name: Fukazawa, Yugo
last_name: Fukazawa
citation:
ama: Luján R, Aguado C, Ciruela F, et al. Sk2 channels associate with mGlu1α receptors
and CaV2.1 channels in Purkinje cells. Frontiers in Cellular Neuroscience.
2018;12. doi:10.3389/fncel.2018.00311
apa: Luján, R., Aguado, C., Ciruela, F., Arus, X., Martín Belmonte, A., Alfaro Ruiz,
R., … Fukazawa, Y. (2018). Sk2 channels associate with mGlu1α receptors and CaV2.1
channels in Purkinje cells. Frontiers in Cellular Neuroscience. Frontiers
Media. https://doi.org/10.3389/fncel.2018.00311
chicago: Luján, Rafæl, Carolina Aguado, Francisco Ciruela, Xavier Arus, Alejandro
Martín Belmonte, Rocío Alfaro Ruiz, Jesus Martinez Gomez, et al. “Sk2 Channels
Associate with MGlu1α Receptors and CaV2.1 Channels in Purkinje Cells.” Frontiers
in Cellular Neuroscience. Frontiers Media, 2018. https://doi.org/10.3389/fncel.2018.00311.
ieee: R. Luján et al., “Sk2 channels associate with mGlu1α receptors and
CaV2.1 channels in Purkinje cells,” Frontiers in Cellular Neuroscience,
vol. 12. Frontiers Media, 2018.
ista: Luján R, Aguado C, Ciruela F, Arus X, Martín Belmonte A, Alfaro Ruiz R, Martinez
Gomez J, De La Ossa L, Watanabe M, Adelman J, Shigemoto R, Fukazawa Y. 2018. Sk2
channels associate with mGlu1α receptors and CaV2.1 channels in Purkinje cells.
Frontiers in Cellular Neuroscience. 12, 311.
mla: Luján, Rafæl, et al. “Sk2 Channels Associate with MGlu1α Receptors and CaV2.1
Channels in Purkinje Cells.” Frontiers in Cellular Neuroscience, vol. 12,
311, Frontiers Media, 2018, doi:10.3389/fncel.2018.00311.
short: R. Luján, C. Aguado, F. Ciruela, X. Arus, A. Martín Belmonte, R. Alfaro Ruiz,
J. Martinez Gomez, L. De La Ossa, M. Watanabe, J. Adelman, R. Shigemoto, Y. Fukazawa,
Frontiers in Cellular Neuroscience 12 (2018).
date_created: 2018-12-11T11:44:19Z
date_published: 2018-09-19T00:00:00Z
date_updated: 2023-09-18T09:31:18Z
day: '19'
ddc:
- '570'
department:
- _id: RySh
doi: 10.3389/fncel.2018.00311
ec_funded: 1
external_id:
isi:
- '000445090100002'
file:
- access_level: open_access
checksum: 0bcaec8d596162af0b7fe3f31325d480
content_type: application/pdf
creator: dernst
date_created: 2018-12-17T08:49:03Z
date_updated: 2020-07-14T12:46:23Z
file_id: '5684'
file_name: fncel-12-00311.pdf
file_size: 6834251
relation: main_file
file_date_updated: 2020-07-14T12:46:23Z
has_accepted_license: '1'
intvolume: ' 12'
isi: 1
language:
- iso: eng
month: '09'
oa: 1
oa_version: Published Version
project:
- _id: 25CBA828-B435-11E9-9278-68D0E5697425
call_identifier: H2020
grant_number: '720270'
name: Human Brain Project Specific Grant Agreement 1 (HBP SGA 1)
publication: Frontiers in Cellular Neuroscience
publication_identifier:
issn:
- '16625102'
publication_status: published
publisher: Frontiers Media
publist_id: '8013'
quality_controlled: '1'
scopus_import: '1'
status: public
title: Sk2 channels associate with mGlu1α receptors and CaV2.1 channels in Purkinje
cells
tmp:
image: /images/cc_by.png
legal_code_url: https://creativecommons.org/licenses/by/4.0/legalcode
name: Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)
short: CC BY (4.0)
type: journal_article
user_id: c635000d-4b10-11ee-a964-aac5a93f6ac1
volume: 12
year: '2018'
...
---
_id: '1146'
abstract:
- lang: eng
text: 'Aim: The present study was to compare the effects of nicotinic acid and nicotinamide
on the plasma methyl donors, choline and betaine. Methods: Thirty adult subjects
were randomly divided into three groups of equal size, and orally received purified
water (C group), nicotinic acid (300 mg, NA group) or nicotinamide (300 mg, NM
group). Plasma nicotinamide, N 1-methylnicotinamide, homocysteine, betaine and
choline levels before and 1.5-h and 3-h post-dosing, plasma normetanephrine and
metanephrine concentrations at 3-h post-dosing, and the urinary excretion of N
1-methyl-2-pyridone-5-carboxamide during the test period were examined. Results:
The level of 3-h plasma nicotinamide, N 1-methylnicotinamide, homocysteine, the
urinary excretion of N 1-methyl-2-pyridone-5-carboxamide and pulse pressure (PP)
in the NM group was 221%, 3972%, 61%, 1728% and 21.2% higher than that of the
control group (P < 0.01, except homocysteine and PP P < 0.05), while the
3-h plasma betaine, normetanephrine and metanephrine level in the NM group was
24.4%, 9.4% and 11.7% lower (P < 0.05, except betaine P < 0.01), without
significant difference in choline levels. Similar but less pronounced changes
were observed in the NA group, with a lower level of 3-h plasma N 1-methylnicotinamide
(1.90 ± 0.20 μmol/l vs. 3.62 ± 0.27 μmol/l, P < 0.01) and homocysteine (12.85
± 1.39 μmol/l vs. 18.08 ± 1.02 μmol/l, P < 0.05) but a higher level of betaine
(27.44 ± 0.71 μmol/l vs. 23.52 ± 0.61 μmol/l, P < 0.05) than that of the NM
group. Conclusion: The degradation of nicotinamide consumes more betaine than
that of nicotinic acid at identical doses. This difference should be taken into
consideration in niacin fortification. © 2016 Elsevier Ltd and European Society
for Clinical Nutrition and Metabolism.'
acknowledgement: We thank all the participants for their contribution to this study
and volunteers from the Nursing School of Dalian University for their supporting
to collect blood and urine samples of the participants. We also thank Dr. Yasunori
Takayama from National Institute for Physiological Sciences of Japan for his kind
help.
article_processing_charge: No
author:
- first_name: Wuping
full_name: Sun, Wuping
last_name: Sun
- first_name: Ming-Zhu
full_name: Zhai, Ming-Zhu
id: 34009CFA-F248-11E8-B48F-1D18A9856A87
last_name: Zhai
- first_name: Da
full_name: Li, Da
last_name: Li
- first_name: Yiming
full_name: Zhou, Yiming
last_name: Zhou
- first_name: Nana
full_name: Chen, Nana
last_name: Chen
- first_name: Ming
full_name: Guo, Ming
last_name: Guo
- first_name: Shisheng
full_name: Zhou, Shisheng
last_name: Zhou
citation:
ama: Sun W, Zhai M-Z, Li D, et al. Comparison of the effects of nicotinic acid and
nicotinamide degradation on plasma betaine and choline levels. Clinical Nutrition.
2017;36(4):1136-1142. doi:10.1016/j.clnu.2016.07.016
apa: Sun, W., Zhai, M.-Z., Li, D., Zhou, Y., Chen, N., Guo, M., & Zhou, S. (2017).
Comparison of the effects of nicotinic acid and nicotinamide degradation on plasma
betaine and choline levels. Clinical Nutrition. Elsevier. https://doi.org/10.1016/j.clnu.2016.07.016
chicago: Sun, Wuping, Ming-Zhu Zhai, Da Li, Yiming Zhou, Nana Chen, Ming Guo, and
Shisheng Zhou. “Comparison of the Effects of Nicotinic Acid and Nicotinamide Degradation
on Plasma Betaine and Choline Levels.” Clinical Nutrition. Elsevier, 2017.
https://doi.org/10.1016/j.clnu.2016.07.016.
ieee: W. Sun et al., “Comparison of the effects of nicotinic acid and nicotinamide
degradation on plasma betaine and choline levels,” Clinical Nutrition,
vol. 36, no. 4. Elsevier, pp. 1136–1142, 2017.
ista: Sun W, Zhai M-Z, Li D, Zhou Y, Chen N, Guo M, Zhou S. 2017. Comparison of
the effects of nicotinic acid and nicotinamide degradation on plasma betaine and
choline levels. Clinical Nutrition. 36(4), 1136–1142.
mla: Sun, Wuping, et al. “Comparison of the Effects of Nicotinic Acid and Nicotinamide
Degradation on Plasma Betaine and Choline Levels.” Clinical Nutrition,
vol. 36, no. 4, Elsevier, 2017, pp. 1136–42, doi:10.1016/j.clnu.2016.07.016.
short: W. Sun, M.-Z. Zhai, D. Li, Y. Zhou, N. Chen, M. Guo, S. Zhou, Clinical Nutrition
36 (2017) 1136–1142.
date_created: 2018-12-11T11:50:24Z
date_published: 2017-08-01T00:00:00Z
date_updated: 2023-10-16T11:09:39Z
day: '01'
department:
- _id: RySh
doi: 10.1016/j.clnu.2016.07.016
intvolume: ' 36'
issue: '4'
language:
- iso: eng
month: '08'
oa_version: None
page: 1136-1142
publication: Clinical Nutrition
publication_identifier:
issn:
- 0261-5614
publication_status: published
publisher: Elsevier
publist_id: '6212'
quality_controlled: '1'
scopus_import: '1'
status: public
title: Comparison of the effects of nicotinic acid and nicotinamide degradation on
plasma betaine and choline levels
type: journal_article
user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87
volume: 36
year: '2017'
...
---
_id: '682'
abstract:
- lang: eng
text: Left-right asymmetry is a fundamental feature of higher-order brain structure;
however, the molecular basis of brain asymmetry remains unclear. We recently identified
structural and functional asymmetries in mouse hippocampal circuitry that result
from the asymmetrical distribution of two distinct populations of pyramidal cell
synapses that differ in the density of the NMDA receptor subunit GluRε2 (also
known as NR2B, GRIN2B or GluN2B). By examining the synaptic distribution of ε2
subunits, we previously found that β2-microglobulin-deficient mice, which lack
cell surface expression of the vast majority of major histocompatibility complex
class I (MHCI) proteins, do not exhibit circuit asymmetry. In the present study,
we conducted electrophysiological and anatomical analyses on the hippocampal circuitry
of mice with a knockout of the paired immunoglobulin-like receptor B (PirB), an
MHCI receptor. As in β2-microglobulin-deficient mice, the PirB-deficient hippocampus
lacked circuit asymmetries. This finding that MHCI loss-of-function mice and PirB
knockout mice have identical phenotypes suggests that MHCI signals that produce
hippocampal asymmetries are transduced through PirB. Our results provide evidence
for a critical role of the MHCI/PirB signaling system in the generation of asymmetries
in hippocampal circuitry.
article_number: e0179377
article_type: original
author:
- first_name: Hikari
full_name: Ukai, Hikari
last_name: Ukai
- first_name: Aiko
full_name: Kawahara, Aiko
last_name: Kawahara
- first_name: Keiko
full_name: Hirayama, Keiko
last_name: Hirayama
- first_name: Matthew J
full_name: Case, Matthew J
id: 44B7CA5A-F248-11E8-B48F-1D18A9856A87
last_name: Case
- first_name: Shotaro
full_name: Aino, Shotaro
last_name: Aino
- first_name: Masahiro
full_name: Miyabe, Masahiro
last_name: Miyabe
- first_name: Ken
full_name: Wakita, Ken
last_name: Wakita
- first_name: Ryohei
full_name: Oogi, Ryohei
last_name: Oogi
- first_name: Michiyo
full_name: Kasayuki, Michiyo
last_name: Kasayuki
- first_name: Shihomi
full_name: Kawashima, Shihomi
last_name: Kawashima
- first_name: Shunichi
full_name: Sugimoto, Shunichi
last_name: Sugimoto
- first_name: Kanako
full_name: Chikamatsu, Kanako
last_name: Chikamatsu
- first_name: Noritaka
full_name: Nitta, Noritaka
last_name: Nitta
- first_name: Tsuneyuki
full_name: Koga, Tsuneyuki
last_name: Koga
- first_name: Ryuichi
full_name: Shigemoto, Ryuichi
id: 499F3ABC-F248-11E8-B48F-1D18A9856A87
last_name: Shigemoto
orcid: 0000-0001-8761-9444
- first_name: Toshiyuki
full_name: Takai, Toshiyuki
last_name: Takai
- first_name: Isao
full_name: Ito, Isao
last_name: Ito
citation:
ama: Ukai H, Kawahara A, Hirayama K, et al. PirB regulates asymmetries in hippocampal
circuitry. PLoS One. 2017;12(6). doi:10.1371/journal.pone.0179377
apa: Ukai, H., Kawahara, A., Hirayama, K., Case, M. J., Aino, S., Miyabe, M., …
Ito, I. (2017). PirB regulates asymmetries in hippocampal circuitry. PLoS One.
Public Library of Science. https://doi.org/10.1371/journal.pone.0179377
chicago: Ukai, Hikari, Aiko Kawahara, Keiko Hirayama, Matthew J Case, Shotaro Aino,
Masahiro Miyabe, Ken Wakita, et al. “PirB Regulates Asymmetries in Hippocampal
Circuitry.” PLoS One. Public Library of Science, 2017. https://doi.org/10.1371/journal.pone.0179377.
ieee: H. Ukai et al., “PirB regulates asymmetries in hippocampal circuitry,”
PLoS One, vol. 12, no. 6. Public Library of Science, 2017.
ista: Ukai H, Kawahara A, Hirayama K, Case MJ, Aino S, Miyabe M, Wakita K, Oogi
R, Kasayuki M, Kawashima S, Sugimoto S, Chikamatsu K, Nitta N, Koga T, Shigemoto
R, Takai T, Ito I. 2017. PirB regulates asymmetries in hippocampal circuitry.
PLoS One. 12(6), e0179377.
mla: Ukai, Hikari, et al. “PirB Regulates Asymmetries in Hippocampal Circuitry.”
PLoS One, vol. 12, no. 6, e0179377, Public Library of Science, 2017, doi:10.1371/journal.pone.0179377.
short: H. Ukai, A. Kawahara, K. Hirayama, M.J. Case, S. Aino, M. Miyabe, K. Wakita,
R. Oogi, M. Kasayuki, S. Kawashima, S. Sugimoto, K. Chikamatsu, N. Nitta, T. Koga,
R. Shigemoto, T. Takai, I. Ito, PLoS One 12 (2017).
date_created: 2018-12-11T11:47:54Z
date_published: 2017-06-01T00:00:00Z
date_updated: 2024-03-25T23:30:07Z
day: '01'
ddc:
- '571'
department:
- _id: RySh
doi: 10.1371/journal.pone.0179377
file:
- access_level: open_access
checksum: 24dd19c46fb1c761b0bcbbcd1025a3a8
content_type: application/pdf
creator: system
date_created: 2018-12-12T10:12:16Z
date_updated: 2020-07-14T12:47:40Z
file_id: '4934'
file_name: IST-2017-897-v1+1_journal.pone.0179377.pdf
file_size: 5798454
relation: main_file
file_date_updated: 2020-07-14T12:47:40Z
has_accepted_license: '1'
intvolume: ' 12'
issue: '6'
language:
- iso: eng
month: '06'
oa: 1
oa_version: Published Version
publication: PLoS One
publication_identifier:
issn:
- '19326203'
publication_status: published
publisher: Public Library of Science
publist_id: '7034'
pubrep_id: '897'
quality_controlled: '1'
related_material:
record:
- id: '51'
relation: dissertation_contains
status: public
scopus_import: 1
status: public
title: PirB regulates asymmetries in hippocampal circuitry
tmp:
image: /images/cc_by.png
legal_code_url: https://creativecommons.org/licenses/by/4.0/legalcode
name: Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)
short: CC BY (4.0)
type: journal_article
user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87
volume: 12
year: '2017'
...
---
_id: '693'
abstract:
- lang: eng
text: 'Many central synapses contain a single presynaptic active zone and a single
postsynaptic density. Vesicular release statistics at such “simple synapses” indicate
that they contain a small complement of docking sites where vesicles repetitively
dock and fuse. In this work, we investigate functional and morphological aspects
of docking sites at simple synapses made between cerebellar parallel fibers and
molecular layer interneurons. Using immunogold labeling of SDS-treated freeze-fracture
replicas, we find that Cav2.1 channels form several clusters per active zone with
about nine channels per cluster. The mean value and range of intersynaptic variation
are similar for Cav2.1 cluster numbers and for functional estimates of docking-site
numbers obtained from the maximum numbers of released vesicles per action potential.
Both numbers grow in relation with synaptic size and decrease by a similar extent
with age between 2 wk and 4 wk postnatal. Thus, the mean docking-site numbers
were 3.15 at 2 wk (range: 1–10) and 2.03 at 4 wk (range: 1–4), whereas the mean
numbers of Cav2.1 clusters were 2.84 at 2 wk (range: 1–8) and 2.37 at 4 wk (range:
1–5). These changes were accompanied by decreases of miniature current amplitude
(from 93 pA to 56 pA), active-zone surface area (from 0.0427 μm2 to 0.0234 μm2),
and initial success rate (from 0.609 to 0.353), indicating a tightening of synaptic
transmission with development. Altogether, these results suggest a close correspondence
between the number of functionally defined vesicular docking sites and that of
clusters of voltage-gated calcium channels. '
article_processing_charge: Yes (in subscription journal)
author:
- first_name: Takafumi
full_name: Miki, Takafumi
last_name: Miki
- first_name: Walter
full_name: Kaufmann, Walter
id: 3F99E422-F248-11E8-B48F-1D18A9856A87
last_name: Kaufmann
orcid: 0000-0001-9735-5315
- first_name: Gerardo
full_name: Malagon, Gerardo
last_name: Malagon
- first_name: Laura
full_name: Gomez, Laura
last_name: Gomez
- first_name: Katsuhiko
full_name: Tabuchi, Katsuhiko
last_name: Tabuchi
- first_name: Masahiko
full_name: Watanabe, Masahiko
last_name: Watanabe
- first_name: Ryuichi
full_name: Shigemoto, Ryuichi
id: 499F3ABC-F248-11E8-B48F-1D18A9856A87
last_name: Shigemoto
orcid: 0000-0001-8761-9444
- first_name: Alain
full_name: Marty, Alain
last_name: Marty
citation:
ama: Miki T, Kaufmann W, Malagon G, et al. Numbers of presynaptic Ca2+ channel clusters
match those of functionally defined vesicular docking sites in single central
synapses. PNAS. 2017;114(26):E5246-E5255. doi:10.1073/pnas.1704470114
apa: Miki, T., Kaufmann, W., Malagon, G., Gomez, L., Tabuchi, K., Watanabe, M.,
… Marty, A. (2017). Numbers of presynaptic Ca2+ channel clusters match those of
functionally defined vesicular docking sites in single central synapses. PNAS.
National Academy of Sciences. https://doi.org/10.1073/pnas.1704470114
chicago: Miki, Takafumi, Walter Kaufmann, Gerardo Malagon, Laura Gomez, Katsuhiko
Tabuchi, Masahiko Watanabe, Ryuichi Shigemoto, and Alain Marty. “Numbers of Presynaptic
Ca2+ Channel Clusters Match Those of Functionally Defined Vesicular Docking Sites
in Single Central Synapses.” PNAS. National Academy of Sciences, 2017.
https://doi.org/10.1073/pnas.1704470114.
ieee: T. Miki et al., “Numbers of presynaptic Ca2+ channel clusters match
those of functionally defined vesicular docking sites in single central synapses,”
PNAS, vol. 114, no. 26. National Academy of Sciences, pp. E5246–E5255,
2017.
ista: Miki T, Kaufmann W, Malagon G, Gomez L, Tabuchi K, Watanabe M, Shigemoto R,
Marty A. 2017. Numbers of presynaptic Ca2+ channel clusters match those of functionally
defined vesicular docking sites in single central synapses. PNAS. 114(26), E5246–E5255.
mla: Miki, Takafumi, et al. “Numbers of Presynaptic Ca2+ Channel Clusters Match
Those of Functionally Defined Vesicular Docking Sites in Single Central Synapses.”
PNAS, vol. 114, no. 26, National Academy of Sciences, 2017, pp. E5246–55,
doi:10.1073/pnas.1704470114.
short: T. Miki, W. Kaufmann, G. Malagon, L. Gomez, K. Tabuchi, M. Watanabe, R. Shigemoto,
A. Marty, PNAS 114 (2017) E5246–E5255.
date_created: 2018-12-11T11:47:57Z
date_published: 2017-06-27T00:00:00Z
date_updated: 2023-02-23T12:54:57Z
day: '27'
ddc:
- '570'
department:
- _id: EM-Fac
- _id: RySh
doi: 10.1073/pnas.1704470114
external_id:
pmid:
- '28607047'
file:
- access_level: open_access
checksum: 2ab75d554f3df4a34d20fa8040589b7e
content_type: application/pdf
creator: kschuh
date_created: 2020-01-03T13:27:29Z
date_updated: 2020-07-14T12:47:44Z
file_id: '7223'
file_name: 2017_PNAS_Miki.pdf
file_size: 2721544
relation: main_file
file_date_updated: 2020-07-14T12:47:44Z
has_accepted_license: '1'
intvolume: ' 114'
issue: '26'
language:
- iso: eng
month: '06'
oa: 1
oa_version: Published Version
page: E5246 - E5255
pmid: 1
publication: PNAS
publication_identifier:
issn:
- '00278424'
publication_status: published
publisher: National Academy of Sciences
publist_id: '7013'
quality_controlled: '1'
scopus_import: 1
status: public
title: Numbers of presynaptic Ca2+ channel clusters match those of functionally defined
vesicular docking sites in single central synapses
type: journal_article
user_id: 3E5EF7F0-F248-11E8-B48F-1D18A9856A87
volume: 114
year: '2017'
...
---
_id: '709'
abstract:
- lang: eng
text: Adipose tissues play key roles in energy homeostasis. Brown adipocytes and
beige adipocytes in white adipose tissue (WAT) share the similar characters of
thermogenesis, both of them could be potential targets for obesity management.
Several thermo-sensitive transient receptor potential channels (thermoTRPs) are
shown to be involved in adipocyte biology. However, the expression pattern of
thermoTRPs in adipose tissues from obese mice is still unknown. The mRNA expression
of thermoTRPs in subcutaneous WAT (sWAT) and interscapular brown adipose tissue
(iBAT) from lean and obese mice were measured using reverse transcriptase-quantitative
PCRs (RT-qPCR). The results demonstrated that all 10 thermoTRPs are expressed
in both iBAT and sWAT, and without significant difference in the mRNA expression
level of thermoTRPs between these two tissues. Moreover, Trpv1 and Trpv3 mRNA
expression levels in both iBAT and sWAT were significantly decreased in high fat
diet (HFD)-induced obese mice and db/db (leptin receptor deficient) mice. Trpm2
mRNA expression level was significantly decreased only in sWAT from HFD-induced
obese mice and db/db mice. On the other hand, Trpv2 and Trpv4 mRNA expression
levels in iBAT and sWAT were significantly increased in HFD-induced obese mice
and db/db mice. Taken together, we conclude that all 10 thermoTRPs are expressed
in iBAT and sWAT. And several thermoTRPs differentially expressed in adipose tissues
from HFD-induced obese mice and db/db mice, suggesting a potential involvement
in anti-obesity regulations.
author:
- first_name: Wuping
full_name: Sun, Wuping
last_name: Sun
- first_name: Chen
full_name: Li, Chen
last_name: Li
- first_name: Yonghong
full_name: Zhang, Yonghong
last_name: Zhang
- first_name: Changyu
full_name: Jiang, Changyu
last_name: Jiang
- first_name: Ming-Zhu
full_name: Zhai, Ming-Zhu
id: 34009CFA-F248-11E8-B48F-1D18A9856A87
last_name: Zhai
- first_name: Qian
full_name: Zhou, Qian
last_name: Zhou
- first_name: Lizu
full_name: Xiao, Lizu
last_name: Xiao
- first_name: Qiwen
full_name: Deng, Qiwen
last_name: Deng
citation:
ama: Sun W, Li C, Zhang Y, et al. Gene expression changes of thermo sensitive transient
receptor potential channels in obese mice. Cell Biology International.
2017;41(8):908-913. doi:10.1002/cbin.10783
apa: Sun, W., Li, C., Zhang, Y., Jiang, C., Zhai, M.-Z., Zhou, Q., … Deng, Q. (2017).
Gene expression changes of thermo sensitive transient receptor potential channels
in obese mice. Cell Biology International. Wiley-Blackwell. https://doi.org/10.1002/cbin.10783
chicago: Sun, Wuping, Chen Li, Yonghong Zhang, Changyu Jiang, Ming-Zhu Zhai, Qian
Zhou, Lizu Xiao, and Qiwen Deng. “Gene Expression Changes of Thermo Sensitive
Transient Receptor Potential Channels in Obese Mice.” Cell Biology International.
Wiley-Blackwell, 2017. https://doi.org/10.1002/cbin.10783.
ieee: W. Sun et al., “Gene expression changes of thermo sensitive transient
receptor potential channels in obese mice,” Cell Biology International,
vol. 41, no. 8. Wiley-Blackwell, pp. 908–913, 2017.
ista: Sun W, Li C, Zhang Y, Jiang C, Zhai M-Z, Zhou Q, Xiao L, Deng Q. 2017. Gene
expression changes of thermo sensitive transient receptor potential channels in
obese mice. Cell Biology International. 41(8), 908–913.
mla: Sun, Wuping, et al. “Gene Expression Changes of Thermo Sensitive Transient
Receptor Potential Channels in Obese Mice.” Cell Biology International,
vol. 41, no. 8, Wiley-Blackwell, 2017, pp. 908–13, doi:10.1002/cbin.10783.
short: W. Sun, C. Li, Y. Zhang, C. Jiang, M.-Z. Zhai, Q. Zhou, L. Xiao, Q. Deng,
Cell Biology International 41 (2017) 908–913.
date_created: 2018-12-11T11:48:04Z
date_published: 2017-08-01T00:00:00Z
date_updated: 2021-01-12T08:11:47Z
day: '01'
department:
- _id: RySh
doi: 10.1002/cbin.10783
intvolume: ' 41'
issue: '8'
language:
- iso: eng
month: '08'
oa_version: None
page: 908 - 913
publication: Cell Biology International
publication_identifier:
issn:
- '10656995'
publication_status: published
publisher: Wiley-Blackwell
publist_id: '6981'
quality_controlled: '1'
scopus_import: 1
status: public
title: Gene expression changes of thermo sensitive transient receptor potential channels
in obese mice
type: journal_article
user_id: 3E5EF7F0-F248-11E8-B48F-1D18A9856A87
volume: 41
year: '2017'
...
---
_id: '736'
abstract:
- lang: eng
text: The neurotransmitter receptor subtype, number, density, and distribution relative
to the location of transmitter release sites are key determinants of signal transmission.
AMPA-type ionotropic glutamate receptors (AMPARs) containing GluA3 and GluA4 subunits
are prominently expressed in subsets of neurons capable of firing action potentials
at high frequencies, such as auditory relay neurons. The auditory nerve (AN) forms
glutamatergic synapses on two types of relay neurons, bushy cells (BCs) and fusiform
cells (FCs) of the cochlear nucleus. AN-BC and AN-FC synapses have distinct kinetics;
thus, we investigated whether the number, density, and localization of GluA3 and
GluA4 subunits in these synapses are differentially organized using quantitative
freeze-fracture replica immunogold labeling. We identify a positive correlation
between the number of AMPARs and the size of AN-BC and AN-FC synapses. Both types
of AN synapses have similar numbers of AMPARs; however, the AN-BC have a higher
density of AMPARs than AN-FC synapses, because the AN-BC synapses are smaller.
A higher number and density of GluA3 subunits are observed at AN-BC synapses,
whereas a higher number and density of GluA4 subunits are observed at AN-FC synapses.
The intrasynaptic distribution of immunogold labeling revealed that AMPAR subunits,
particularly GluA3, are concentrated at the center of the AN-BC synapses. The
central distribution of AMPARs is absent in GluA3-knockout mice, and gold particles
are evenly distributed along the postsynaptic density. GluA4 gold labeling was
homogenously distributed along both synapse types. Thus, GluA3 and GluA4 subunits
are distributed at AN synapses in a target-cell-dependent manner.
article_processing_charge: No
author:
- first_name: María
full_name: Rubio, María
last_name: Rubio
- first_name: Ko
full_name: Matsui, Ko
last_name: Matsui
- first_name: Yugo
full_name: Fukazawa, Yugo
last_name: Fukazawa
- first_name: Naomi
full_name: Kamasawa, Naomi
last_name: Kamasawa
- first_name: Harumi
full_name: Harada, Harumi
id: 2E55CDF2-F248-11E8-B48F-1D18A9856A87
last_name: Harada
orcid: 0000-0001-7429-7896
- first_name: Makoto
full_name: Itakura, Makoto
last_name: Itakura
- first_name: Elek
full_name: Molnár, Elek
last_name: Molnár
- first_name: Manabu
full_name: Abe, Manabu
last_name: Abe
- first_name: Kenji
full_name: Sakimura, Kenji
last_name: Sakimura
- first_name: Ryuichi
full_name: Shigemoto, Ryuichi
id: 499F3ABC-F248-11E8-B48F-1D18A9856A87
last_name: Shigemoto
orcid: 0000-0001-8761-9444
citation:
ama: Rubio M, Matsui K, Fukazawa Y, et al. The number and distribution of AMPA receptor
channels containing fast kinetic GluA3 and GluA4 subunits at auditory nerve synapses
depend on the target cells. Brain Structure and Function. 2017;222(8):3375-3393.
doi:10.1007/s00429-017-1408-0
apa: Rubio, M., Matsui, K., Fukazawa, Y., Kamasawa, N., Harada, H., Itakura, M.,
… Shigemoto, R. (2017). The number and distribution of AMPA receptor channels
containing fast kinetic GluA3 and GluA4 subunits at auditory nerve synapses depend
on the target cells. Brain Structure and Function. Springer. https://doi.org/10.1007/s00429-017-1408-0
chicago: Rubio, María, Ko Matsui, Yugo Fukazawa, Naomi Kamasawa, Harumi Harada,
Makoto Itakura, Elek Molnár, Manabu Abe, Kenji Sakimura, and Ryuichi Shigemoto.
“The Number and Distribution of AMPA Receptor Channels Containing Fast Kinetic
GluA3 and GluA4 Subunits at Auditory Nerve Synapses Depend on the Target Cells.”
Brain Structure and Function. Springer, 2017. https://doi.org/10.1007/s00429-017-1408-0.
ieee: M. Rubio et al., “The number and distribution of AMPA receptor channels
containing fast kinetic GluA3 and GluA4 subunits at auditory nerve synapses depend
on the target cells,” Brain Structure and Function, vol. 222, no. 8. Springer,
pp. 3375–3393, 2017.
ista: Rubio M, Matsui K, Fukazawa Y, Kamasawa N, Harada H, Itakura M, Molnár E,
Abe M, Sakimura K, Shigemoto R. 2017. The number and distribution of AMPA receptor
channels containing fast kinetic GluA3 and GluA4 subunits at auditory nerve synapses
depend on the target cells. Brain Structure and Function. 222(8), 3375–3393.
mla: Rubio, María, et al. “The Number and Distribution of AMPA Receptor Channels
Containing Fast Kinetic GluA3 and GluA4 Subunits at Auditory Nerve Synapses Depend
on the Target Cells.” Brain Structure and Function, vol. 222, no. 8, Springer,
2017, pp. 3375–93, doi:10.1007/s00429-017-1408-0.
short: M. Rubio, K. Matsui, Y. Fukazawa, N. Kamasawa, H. Harada, M. Itakura, E.
Molnár, M. Abe, K. Sakimura, R. Shigemoto, Brain Structure and Function 222 (2017)
3375–3393.
date_created: 2018-12-11T11:48:14Z
date_published: 2017-11-01T00:00:00Z
date_updated: 2023-09-27T14:14:51Z
day: '01'
ddc:
- '571'
department:
- _id: RySh
doi: 10.1007/s00429-017-1408-0
external_id:
isi:
- '000414761700002'
file:
- access_level: open_access
checksum: 73787a22507de8fb585bb598e1418ca7
content_type: application/pdf
creator: system
date_created: 2018-12-12T10:10:20Z
date_updated: 2020-07-14T12:47:56Z
file_id: '4806'
file_name: IST-2017-881-v1+1_s00429-017-1408-0.pdf
file_size: 4011126
relation: main_file
file_date_updated: 2020-07-14T12:47:56Z
has_accepted_license: '1'
intvolume: ' 222'
isi: 1
issue: '8'
language:
- iso: eng
month: '11'
oa: 1
oa_version: Published Version
page: 3375 - 3393
publication: Brain Structure and Function
publication_identifier:
issn:
- '18632653'
publication_status: published
publisher: Springer
publist_id: '6932'
pubrep_id: '881'
quality_controlled: '1'
scopus_import: '1'
status: public
title: The number and distribution of AMPA receptor channels containing fast kinetic
GluA3 and GluA4 subunits at auditory nerve synapses depend on the target cells
tmp:
image: /images/cc_by.png
legal_code_url: https://creativecommons.org/licenses/by/4.0/legalcode
name: Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)
short: CC BY (4.0)
type: journal_article
user_id: c635000d-4b10-11ee-a964-aac5a93f6ac1
volume: 222
year: '2017'
...
---
_id: '740'
abstract:
- lang: eng
text: 'Developments in bioengineering and molecular biology have introduced a palette
of genetically encoded probes for identification of specific cell populations
in electron microscopy. These probes can be targeted to distinct cellular compartments,
rendering them electron dense through a subsequent chemical reaction. These electron
densities strongly increase the local contrast in samples prepared for electron
microscopy, allowing three major advances in ultrastructural mapping of circuits:
genetic identification of circuit components, targeted imaging of regions of interest
and automated analysis of the tagged circuits. Together, the gains from these
advances can decrease the time required for the analysis of targeted circuit motifs
by over two orders of magnitude. These genetic encoded tags for electron microscopy
promise to simplify the analysis of circuit motifs and become a central tool for
structure‐function studies of synaptic connections in the brain. We review the
current state‐of‐the‐art with an emphasis on connectomics, the quantitative analysis
of neuronal structures and motifs.'
article_number: e288
article_processing_charge: No
article_type: original
author:
- first_name: Ryuichi
full_name: Shigemoto, Ryuichi
id: 499F3ABC-F248-11E8-B48F-1D18A9856A87
last_name: Shigemoto
orcid: 0000-0001-8761-9444
- first_name: Maximilian A
full_name: Jösch, Maximilian A
id: 2BD278E6-F248-11E8-B48F-1D18A9856A87
last_name: Jösch
orcid: 0000-0002-3937-1330
citation:
ama: Shigemoto R, Jösch MA. The genetic encoded toolbox for electron microscopy
and connectomics. WIREs Developmental Biology. 2017;6(6). doi:10.1002/wdev.288
apa: Shigemoto, R., & Jösch, M. A. (2017). The genetic encoded toolbox for electron
microscopy and connectomics. WIREs Developmental Biology. Wiley-Blackwell.
https://doi.org/10.1002/wdev.288
chicago: Shigemoto, Ryuichi, and Maximilian A Jösch. “The Genetic Encoded Toolbox
for Electron Microscopy and Connectomics.” WIREs Developmental Biology.
Wiley-Blackwell, 2017. https://doi.org/10.1002/wdev.288.
ieee: R. Shigemoto and M. A. Jösch, “The genetic encoded toolbox for electron microscopy
and connectomics,” WIREs Developmental Biology, vol. 6, no. 6. Wiley-Blackwell,
2017.
ista: Shigemoto R, Jösch MA. 2017. The genetic encoded toolbox for electron microscopy
and connectomics. WIREs Developmental Biology. 6(6), e288.
mla: Shigemoto, Ryuichi, and Maximilian A. Jösch. “The Genetic Encoded Toolbox for
Electron Microscopy and Connectomics.” WIREs Developmental Biology, vol.
6, no. 6, e288, Wiley-Blackwell, 2017, doi:10.1002/wdev.288.
short: R. Shigemoto, M.A. Jösch, WIREs Developmental Biology 6 (2017).
date_created: 2018-12-11T11:48:15Z
date_published: 2017-08-11T00:00:00Z
date_updated: 2023-09-27T12:51:41Z
day: '11'
ddc:
- '570'
department:
- _id: RySh
- _id: MaJö
doi: 10.1002/wdev.288
external_id:
isi:
- '000412827400005'
pmid:
- '28800674'
file:
- access_level: open_access
checksum: a9370f27b1591773b7a0de299bc81c8c
content_type: application/pdf
creator: dernst
date_created: 2019-11-19T07:36:18Z
date_updated: 2020-07-14T12:47:57Z
file_id: '7045'
file_name: 2017_WIREs_Shigemoto.pdf
file_size: 1647787
relation: main_file
file_date_updated: 2020-07-14T12:47:57Z
has_accepted_license: '1'
intvolume: ' 6'
isi: 1
issue: '6'
language:
- iso: eng
license: https://creativecommons.org/licenses/by-nc/4.0/
month: '08'
oa: 1
oa_version: Submitted Version
pmid: 1
publication: WIREs Developmental Biology
publication_identifier:
issn:
- '17597684'
publication_status: published
publisher: Wiley-Blackwell
publist_id: '6927'
quality_controlled: '1'
scopus_import: '1'
status: public
title: The genetic encoded toolbox for electron microscopy and connectomics
tmp:
image: /images/cc_by_nc.png
legal_code_url: https://creativecommons.org/licenses/by-nc/4.0/legalcode
name: Creative Commons Attribution-NonCommercial 4.0 International (CC BY-NC 4.0)
short: CC BY-NC (4.0)
type: journal_article
user_id: c635000d-4b10-11ee-a964-aac5a93f6ac1
volume: 6
year: '2017'
...
---
_id: '746'
abstract:
- lang: eng
text: Metabotropic glutamate receptor subtype 5 (mGluR5) is crucially implicated
in the pathophysiology of Fragile X Syndrome (FXS); however, its dysfunction at
the sub-cellular level, and related synaptic and cognitive phenotypes are unexplored.
Here, we probed the consequences of mGluR5/Homer scaffold disruption for mGluR5
cell-surface mobility, synaptic N-methyl-D-Aspartate receptor (NMDAR) function,
and behavioral phenotypes in the second-generation Fmr1 knockout (KO) mouse. Using
single-molecule tracking, we found that mGluR5 was significantly more mobile at
synapses in hippocampal Fmr1 KO neurons, causing an increased synaptic surface
co-clustering of mGluR5 and NMDAR. This correlated with a reduced amplitude of
synaptic NMDAR currents, a lack of their mGluR5-Activated long-Term depression,
and NMDAR/hippocampus dependent cognitive deficits. These synaptic and behavioral
phenomena were reversed by knocking down Homer1a in Fmr1 KO mice. Our study provides
a mechanistic link between changes of mGluR5 dynamics and pathological phenotypes
of FXS, unveiling novel targets for mGluR5-based therapeutics.
article_number: '1103'
article_processing_charge: No
author:
- first_name: Elisabetta
full_name: Aloisi, Elisabetta
last_name: Aloisi
- first_name: Katy
full_name: Le Corf, Katy
last_name: Le Corf
- first_name: Julien
full_name: Dupuis, Julien
last_name: Dupuis
- first_name: Pei
full_name: Zhang, Pei
last_name: Zhang
- first_name: Melanie
full_name: Ginger, Melanie
last_name: Ginger
- first_name: Virginie
full_name: Labrousse, Virginie
last_name: Labrousse
- first_name: Michela
full_name: Spatuzza, Michela
last_name: Spatuzza
- first_name: Matthias
full_name: Georg Haberl, Matthias
last_name: Georg Haberl
- first_name: Lara
full_name: Costa, Lara
last_name: Costa
- first_name: Ryuichi
full_name: Shigemoto, Ryuichi
id: 499F3ABC-F248-11E8-B48F-1D18A9856A87
last_name: Shigemoto
orcid: 0000-0001-8761-9444
- first_name: Anke
full_name: Tappe Theodor, Anke
last_name: Tappe Theodor
- first_name: Fillippo
full_name: Drago, Fillippo
last_name: Drago
- first_name: Pier
full_name: Vincenzo Piazza, Pier
last_name: Vincenzo Piazza
- first_name: Christophe
full_name: Mulle, Christophe
last_name: Mulle
- first_name: Laurent
full_name: Groc, Laurent
last_name: Groc
- first_name: Lucia
full_name: Ciranna, Lucia
last_name: Ciranna
- first_name: Maria
full_name: Catania, Maria
last_name: Catania
- first_name: Andreas
full_name: Frick, Andreas
last_name: Frick
citation:
ama: Aloisi E, Le Corf K, Dupuis J, et al. Altered surface mGluR5 dynamics provoke
synaptic NMDAR dysfunction and cognitive defects in Fmr1 knockout mice. Nature
Communications. 2017;8(1). doi:10.1038/s41467-017-01191-2
apa: Aloisi, E., Le Corf, K., Dupuis, J., Zhang, P., Ginger, M., Labrousse, V.,
… Frick, A. (2017). Altered surface mGluR5 dynamics provoke synaptic NMDAR dysfunction
and cognitive defects in Fmr1 knockout mice. Nature Communications. Nature
Publishing Group. https://doi.org/10.1038/s41467-017-01191-2
chicago: Aloisi, Elisabetta, Katy Le Corf, Julien Dupuis, Pei Zhang, Melanie Ginger,
Virginie Labrousse, Michela Spatuzza, et al. “Altered Surface MGluR5 Dynamics
Provoke Synaptic NMDAR Dysfunction and Cognitive Defects in Fmr1 Knockout Mice.”
Nature Communications. Nature Publishing Group, 2017. https://doi.org/10.1038/s41467-017-01191-2.
ieee: E. Aloisi et al., “Altered surface mGluR5 dynamics provoke synaptic
NMDAR dysfunction and cognitive defects in Fmr1 knockout mice,” Nature Communications,
vol. 8, no. 1. Nature Publishing Group, 2017.
ista: Aloisi E, Le Corf K, Dupuis J, Zhang P, Ginger M, Labrousse V, Spatuzza M,
Georg Haberl M, Costa L, Shigemoto R, Tappe Theodor A, Drago F, Vincenzo Piazza
P, Mulle C, Groc L, Ciranna L, Catania M, Frick A. 2017. Altered surface mGluR5
dynamics provoke synaptic NMDAR dysfunction and cognitive defects in Fmr1 knockout
mice. Nature Communications. 8(1), 1103.
mla: Aloisi, Elisabetta, et al. “Altered Surface MGluR5 Dynamics Provoke Synaptic
NMDAR Dysfunction and Cognitive Defects in Fmr1 Knockout Mice.” Nature Communications,
vol. 8, no. 1, 1103, Nature Publishing Group, 2017, doi:10.1038/s41467-017-01191-2.
short: E. Aloisi, K. Le Corf, J. Dupuis, P. Zhang, M. Ginger, V. Labrousse, M. Spatuzza,
M. Georg Haberl, L. Costa, R. Shigemoto, A. Tappe Theodor, F. Drago, P. Vincenzo
Piazza, C. Mulle, L. Groc, L. Ciranna, M. Catania, A. Frick, Nature Communications
8 (2017).
date_created: 2018-12-11T11:48:17Z
date_published: 2017-12-01T00:00:00Z
date_updated: 2023-09-27T12:27:30Z
day: '01'
ddc:
- '571'
department:
- _id: RySh
doi: 10.1038/s41467-017-01191-2
external_id:
isi:
- '000413571300004'
file:
- access_level: open_access
checksum: 99ceee57549dc0461e3adfc037ec70a9
content_type: application/pdf
creator: system
date_created: 2018-12-12T10:17:32Z
date_updated: 2020-07-14T12:47:58Z
file_id: '5287'
file_name: IST-2017-915-v1+1_s41467-017-01191-2.pdf
file_size: 1841650
relation: main_file
file_date_updated: 2020-07-14T12:47:58Z
has_accepted_license: '1'
intvolume: ' 8'
isi: 1
issue: '1'
language:
- iso: eng
month: '12'
oa: 1
oa_version: Published Version
publication: Nature Communications
publication_identifier:
issn:
- '20411723'
publication_status: published
publisher: Nature Publishing Group
publist_id: '6921'
pubrep_id: '915'
quality_controlled: '1'
scopus_import: '1'
status: public
title: Altered surface mGluR5 dynamics provoke synaptic NMDAR dysfunction and cognitive
defects in Fmr1 knockout mice
tmp:
image: /images/cc_by.png
legal_code_url: https://creativecommons.org/licenses/by/4.0/legalcode
name: Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)
short: CC BY (4.0)
type: journal_article
user_id: c635000d-4b10-11ee-a964-aac5a93f6ac1
volume: 8
year: '2017'
...
---
_id: '627'
abstract:
- lang: eng
text: Beige adipocytes are a new type of recruitable brownish adipocytes, with highly
mitochondrial membrane uncoupling protein 1 expression and thermogenesis. Beige
adipocytes were found among white adipocytes, especially in subcutaneous white
adipose tissue (sWAT). Therefore, beige adipocytes may be involved in the regulation
of energy metabolism and fat deposition. Transient receptor potential melastatin
8 (TRPM8), a Ca2+-permeable non-selective cation channel, plays vital roles in
the regulation of various cellular functions. It has been reported that TRPM8
activation enhanced the thermogenic function of brown adiposytes. However, the
involvement of TRPM8 in the thermogenic function of WAT remains unexplored. Our
data revealed that TRPM8 was expressed in mouse white adipocytes at mRNA, protein
and functional levels. The mRNA expression of Trpm8 was significantly increased
in the differentiated white adipocytes than pre-adipocytes. Moreover, activation
of TRPM8 by menthol enhanced the expression of thermogenic genes in cultured white
aidpocytes. And menthol-induced increases of the thermogenic genes in white adipocytes
was inhibited by either KT5720 (a protein kinase A inhibitor) or BAPTA-AM. In
addition, high fat diet (HFD)-induced obesity in mice was significantly recovered
by co-treatment with menthol. Dietary menthol enhanced WAT "browning"
and improved glucose metabolism in HFD-induced obesity mice as well. Therefore,
we concluded that TRPM8 might be involved in WAT "browning" by increasing
the expression levels of genes related to thermogenesis and energy metabolism.
And dietary menthol could be a novel approach for combating human obesity and
related metabolic diseases.
article_processing_charge: No
author:
- first_name: Changyu
full_name: Jiang, Changyu
last_name: Jiang
- first_name: Ming-Zhu
full_name: Zhai, Ming-Zhu
id: 34009CFA-F248-11E8-B48F-1D18A9856A87
last_name: Zhai
- first_name: Dong
full_name: Yan, Dong
last_name: Yan
- first_name: Da
full_name: Li, Da
last_name: Li
- first_name: Chen
full_name: Li, Chen
last_name: Li
- first_name: Yonghong
full_name: Zhang, Yonghong
last_name: Zhang
- first_name: Lizu
full_name: Xiao, Lizu
last_name: Xiao
- first_name: Donglin
full_name: Xiong, Donglin
last_name: Xiong
- first_name: Qiwen
full_name: Deng, Qiwen
last_name: Deng
- first_name: Wuping
full_name: Sun, Wuping
last_name: Sun
citation:
ama: Jiang C, Zhai M-Z, Yan D, et al. Dietary menthol-induced TRPM8 activation enhances
WAT “browning” and ameliorates diet-induced obesity. Oncotarget. 2017;8(43):75114-75126.
doi:10.18632/oncotarget.20540
apa: Jiang, C., Zhai, M.-Z., Yan, D., Li, D., Li, C., Zhang, Y., … Sun, W. (2017).
Dietary menthol-induced TRPM8 activation enhances WAT “browning” and ameliorates
diet-induced obesity. Oncotarget. Impact Journals. https://doi.org/10.18632/oncotarget.20540
chicago: Jiang, Changyu, Ming-Zhu Zhai, Dong Yan, Da Li, Chen Li, Yonghong Zhang,
Lizu Xiao, Donglin Xiong, Qiwen Deng, and Wuping Sun. “Dietary Menthol-Induced
TRPM8 Activation Enhances WAT ‘Browning’ and Ameliorates Diet-Induced Obesity.”
Oncotarget. Impact Journals, 2017. https://doi.org/10.18632/oncotarget.20540.
ieee: C. Jiang et al., “Dietary menthol-induced TRPM8 activation enhances
WAT ‘browning’ and ameliorates diet-induced obesity,” Oncotarget, vol.
8, no. 43. Impact Journals, pp. 75114–75126, 2017.
ista: Jiang C, Zhai M-Z, Yan D, Li D, Li C, Zhang Y, Xiao L, Xiong D, Deng Q, Sun
W. 2017. Dietary menthol-induced TRPM8 activation enhances WAT “browning” and
ameliorates diet-induced obesity. Oncotarget. 8(43), 75114–75126.
mla: Jiang, Changyu, et al. “Dietary Menthol-Induced TRPM8 Activation Enhances WAT
‘Browning’ and Ameliorates Diet-Induced Obesity.” Oncotarget, vol. 8, no.
43, Impact Journals, 2017, pp. 75114–26, doi:10.18632/oncotarget.20540.
short: C. Jiang, M.-Z. Zhai, D. Yan, D. Li, C. Li, Y. Zhang, L. Xiao, D. Xiong,
Q. Deng, W. Sun, Oncotarget 8 (2017) 75114–75126.
date_created: 2018-12-11T11:47:34Z
date_published: 2017-08-24T00:00:00Z
date_updated: 2023-10-17T08:56:37Z
day: '24'
ddc:
- '571'
department:
- _id: RySh
doi: 10.18632/oncotarget.20540
file:
- access_level: open_access
checksum: 2219e5348bbfe1aac2725aa620c33280
content_type: application/pdf
creator: system
date_created: 2018-12-12T10:16:15Z
date_updated: 2020-07-14T12:47:26Z
file_id: '5201'
file_name: IST-2017-907-v1+1_20540-294640-4-PB.pdf
file_size: 6101606
relation: main_file
file_date_updated: 2020-07-14T12:47:26Z
has_accepted_license: '1'
intvolume: ' 8'
issue: '43'
language:
- iso: eng
month: '08'
oa: 1
oa_version: Published Version
page: 75114 - 75126
publication: Oncotarget
publication_identifier:
issn:
- 1949-2553
publication_status: published
publisher: Impact Journals
publist_id: '7167'
pubrep_id: '907'
quality_controlled: '1'
scopus_import: '1'
status: public
title: Dietary menthol-induced TRPM8 activation enhances WAT “browning” and ameliorates
diet-induced obesity
tmp:
image: /images/cc_by.png
legal_code_url: https://creativecommons.org/licenses/by/4.0/legalcode
name: Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)
short: CC BY (4.0)
type: journal_article
user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87
volume: 8
year: '2017'
...
---
_id: '643'
abstract:
- lang: eng
text: It has been reported that nicotinamide-overload induces oxidative stress associated
with insulin resistance, the key feature of type 2 diabetes mellitus (T2DM). This
study aimed to investigate the effects of B vitamins in T2DM. Glucose tolerance
tests (GTT) were carried out in adult Sprague-Dawley rats treated with or without
cumulative doses of B vitamins. More specifically, insulin tolerance tests (ITT)
were also carried out in adult Sprague-Dawley rats treated with or without cumulative
doses of Vitamin B3. We found that cumulative Vitamin B1 and Vitamin B3 administration
significantly increased the plasma H2O2 levels associated with high insulin levels.
Only Vitamin B3 reduced muscular and hepatic glycogen contents. Cumulative administration
of nicotinic acid, another form of Vitamin B3, also significantly increased plasma
insulin level and H2O2 generation. Moreover, cumulative administration of nicotinic
acid or nicotinamide impaired glucose metabolism. This study suggested that excess
Vitamin B1 and Vitamin B3 caused oxidative stress and insulin resistance.
article_processing_charge: No
article_type: original
author:
- first_name: Wuping
full_name: Sun, Wuping
last_name: Sun
- first_name: Ming-Zhu
full_name: Zhai, Ming-Zhu
id: 34009CFA-F248-11E8-B48F-1D18A9856A87
last_name: Zhai
- first_name: Qian
full_name: Zhou, Qian
last_name: Zhou
- first_name: Chengrui
full_name: Qian, Chengrui
last_name: Qian
- first_name: Changyu
full_name: Jiang, Changyu
last_name: Jiang
citation:
ama: Sun W, Zhai M-Z, Zhou Q, Qian C, Jiang C. Effects of B vitamins overload on
plasma insulin level and hydrogen peroxide generation in rats. Chinese Journal
of Physiology. 2017;60(4):207-214. doi:10.4077/CJP.2017.BAF469
apa: Sun, W., Zhai, M.-Z., Zhou, Q., Qian, C., & Jiang, C. (2017). Effects of
B vitamins overload on plasma insulin level and hydrogen peroxide generation in
rats. Chinese Journal of Physiology. Chinese Physiological Society. https://doi.org/10.4077/CJP.2017.BAF469
chicago: Sun, Wuping, Ming-Zhu Zhai, Qian Zhou, Chengrui Qian, and Changyu Jiang.
“Effects of B Vitamins Overload on Plasma Insulin Level and Hydrogen Peroxide
Generation in Rats.” Chinese Journal of Physiology. Chinese Physiological
Society, 2017. https://doi.org/10.4077/CJP.2017.BAF469.
ieee: W. Sun, M.-Z. Zhai, Q. Zhou, C. Qian, and C. Jiang, “Effects of B vitamins
overload on plasma insulin level and hydrogen peroxide generation in rats,” Chinese
Journal of Physiology, vol. 60, no. 4. Chinese Physiological Society, pp.
207–214, 2017.
ista: Sun W, Zhai M-Z, Zhou Q, Qian C, Jiang C. 2017. Effects of B vitamins overload
on plasma insulin level and hydrogen peroxide generation in rats. Chinese Journal
of Physiology. 60(4), 207–214.
mla: Sun, Wuping, et al. “Effects of B Vitamins Overload on Plasma Insulin Level
and Hydrogen Peroxide Generation in Rats.” Chinese Journal of Physiology,
vol. 60, no. 4, Chinese Physiological Society, 2017, pp. 207–14, doi:10.4077/CJP.2017.BAF469.
short: W. Sun, M.-Z. Zhai, Q. Zhou, C. Qian, C. Jiang, Chinese Journal of Physiology
60 (2017) 207–214.
date_created: 2018-12-11T11:47:40Z
date_published: 2017-08-31T00:00:00Z
date_updated: 2021-01-12T08:07:28Z
day: '31'
ddc:
- '570'
department:
- _id: RySh
doi: 10.4077/CJP.2017.BAF469
external_id:
pmid:
- '28847140'
intvolume: ' 60'
issue: '4'
language:
- iso: eng
month: '08'
oa_version: Published Version
page: 207 - 214
pmid: 1
publication: Chinese Journal of Physiology
publication_identifier:
issn:
- '03044920'
publication_status: published
publisher: Chinese Physiological Society
publist_id: '7142'
quality_controlled: '1'
scopus_import: 1
status: public
title: Effects of B vitamins overload on plasma insulin level and hydrogen peroxide
generation in rats
type: journal_article
user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87
volume: 60
year: '2017'
...
---
_id: '1083'
abstract:
- lang: eng
text: ' Cholecystokinin-expressing interneurons (CCK-INs) mediate behavior state-dependent
inhibition in cortical circuits and themselves receive strong GABAergic input.
However, it remains unclear to what extent GABABreceptors (GABABRs) contribute
to their inhibitory control. Using immunoelectron microscopy, we found that CCK-INs
in the rat hippocampus possessed high levels of dendritic GABABRs and KCTD12 auxiliary
proteins, whereas postsynaptic effector Kir3 channels were present at lower levels.
Consistently, whole-cell recordings revealed slow GABABR-mediated inhibitory postsynaptic
currents (IPSCs) in most CCK-INs. In spite of the higher surface density of GABABRs
in CCK-INs than in CA1 principal cells, the amplitudes of IPSCs were comparable,
suggesting that the expression of Kir3 channels is the limiting factor for the
GABABR currents in these INs. Morphological analysis showed that CCK-INs were
diverse, comprising perisomatic-targeting basket cells (BCs), as well as dendrite-targeting
(DT) interneurons, including a previously undescribed DT type. GABABR-mediated
IPSCs in CCK-INs were large in BCs, but small in DT subtypes. In response to prolonged
activation, GABABR-mediated currents displayed strong desensitization, which was
absent in KCTD12-deficient mice. This study highlights that GABABRs differentially
control CCK-IN subtypes, and the kinetics and desensitization of GABABR-mediated
currents are modulated by KCTD12 proteins. '
acknowledgement: "This work was supported by the Deutsche Forschungsgemeinschaft (DFG
SFB 780 A2, A.K.; SFB TR3 I.V. and EXC 257, I.V.; FOR 2143, A.K. and I.V.), Spemann
Graduate School (D.A.), BIOSS-2 (A6, A.K.), the Swiss National Science Foundation
(3100A0-117816, B.B.), The McNaught Bequest (S.A.B. and I.V.), and Tenovus Scotland
(I.V.).\r\n\r\n\r\nWe thank Cheryl Hutton and Chinmaya Sadangi for their contributions
to neuronal reconstruction as well as Natalie Wernet, Sigrun Nestel, Anikó Schneider,
Ina Wolter, and Ulrich Noeller for their excellent technical support. VGAT-Venus
transgenic rats were generated by Drs Y. Yanagawa, M. Hirabayashi, and Y. Kawaguchi
in National Institute for Physiological Sciences, Okazaki, Japan, using pCS2-Venus
provided by Dr A. Miyawaki. The monoclonal mouse CCK antibody was generously provided
by Dr G.V. Ohning, CURE Center, UCLA, CA. "
author:
- first_name: Sam
full_name: Booker, Sam
last_name: Booker
- first_name: Daniel
full_name: Althof, Daniel
last_name: Althof
- first_name: Anna
full_name: Gross, Anna
last_name: Gross
- first_name: Desiree
full_name: Loreth, Desiree
last_name: Loreth
- first_name: Johanna
full_name: Müller, Johanna
last_name: Müller
- first_name: Andreas
full_name: Unger, Andreas
last_name: Unger
- first_name: Bernd
full_name: Fakler, Bernd
last_name: Fakler
- first_name: Andrea
full_name: Varro, Andrea
last_name: Varro
- first_name: Masahiko
full_name: Watanabe, Masahiko
last_name: Watanabe
- first_name: Martin
full_name: Gassmann, Martin
last_name: Gassmann
- first_name: Bernhard
full_name: Bettler, Bernhard
last_name: Bettler
- first_name: Ryuichi
full_name: Shigemoto, Ryuichi
id: 499F3ABC-F248-11E8-B48F-1D18A9856A87
last_name: Shigemoto
orcid: 0000-0001-8761-9444
- first_name: Imre
full_name: Vida, Imre
last_name: Vida
- first_name: Ákos
full_name: Kulik, Ákos
last_name: Kulik
citation:
ama: Booker S, Althof D, Gross A, et al. KCTD12 auxiliary proteins modulate kinetics
of GABAB receptor-mediated inhibition in Cholecystokinin-containing interneurons.
Cerebral Cortex. 2016;27(3):2318-2334. doi:10.1093/cercor/bhw090
apa: Booker, S., Althof, D., Gross, A., Loreth, D., Müller, J., Unger, A., … Kulik,
Á. (2016). KCTD12 auxiliary proteins modulate kinetics of GABAB receptor-mediated
inhibition in Cholecystokinin-containing interneurons. Cerebral Cortex.
Oxford University Press. https://doi.org/10.1093/cercor/bhw090
chicago: Booker, Sam, Daniel Althof, Anna Gross, Desiree Loreth, Johanna Müller,
Andreas Unger, Bernd Fakler, et al. “KCTD12 Auxiliary Proteins Modulate Kinetics
of GABAB Receptor-Mediated Inhibition in Cholecystokinin-Containing Interneurons.”
Cerebral Cortex. Oxford University Press, 2016. https://doi.org/10.1093/cercor/bhw090.
ieee: S. Booker et al., “KCTD12 auxiliary proteins modulate kinetics of GABAB
receptor-mediated inhibition in Cholecystokinin-containing interneurons,” Cerebral
Cortex, vol. 27, no. 3. Oxford University Press, pp. 2318–2334, 2016.
ista: Booker S, Althof D, Gross A, Loreth D, Müller J, Unger A, Fakler B, Varro
A, Watanabe M, Gassmann M, Bettler B, Shigemoto R, Vida I, Kulik Á. 2016. KCTD12
auxiliary proteins modulate kinetics of GABAB receptor-mediated inhibition in
Cholecystokinin-containing interneurons. Cerebral Cortex. 27(3), 2318–2334.
mla: Booker, Sam, et al. “KCTD12 Auxiliary Proteins Modulate Kinetics of GABAB Receptor-Mediated
Inhibition in Cholecystokinin-Containing Interneurons.” Cerebral Cortex,
vol. 27, no. 3, Oxford University Press, 2016, pp. 2318–34, doi:10.1093/cercor/bhw090.
short: S. Booker, D. Althof, A. Gross, D. Loreth, J. Müller, A. Unger, B. Fakler,
A. Varro, M. Watanabe, M. Gassmann, B. Bettler, R. Shigemoto, I. Vida, Á. Kulik,
Cerebral Cortex 27 (2016) 2318–2334.
date_created: 2018-12-11T11:50:03Z
date_published: 2016-04-12T00:00:00Z
date_updated: 2021-01-12T06:48:09Z
day: '12'
department:
- _id: RySh
doi: 10.1093/cercor/bhw090
intvolume: ' 27'
issue: '3'
language:
- iso: eng
month: '04'
oa_version: None
page: 2318 - 2334
publication: Cerebral Cortex
publication_status: published
publisher: Oxford University Press
publist_id: '6297'
quality_controlled: '1'
status: public
title: KCTD12 auxiliary proteins modulate kinetics of GABAB receptor-mediated inhibition
in Cholecystokinin-containing interneurons
type: journal_article
user_id: 3E5EF7F0-F248-11E8-B48F-1D18A9856A87
volume: 27
year: '2016'
...
---
_id: '1094'
abstract:
- lang: eng
text: Immunogold labeling of freeze-fracture replicas has recently been used for
high-resolution visualization of protein localization in electron microscopy.
This method has higher labeling efficiency than conventional immunogold methods
for membrane molecules allowing precise quantitative measurements. However, one
of the limitations of freeze-fracture replica immunolabeling is difficulty in
keeping structural orientation and identifying labeled profiles in complex tissues
like brain. The difficulty is partly due to fragmentation of freeze-fracture replica
preparations during labeling procedures and limited morphological clues on the
replica surface. To overcome these issues, we introduce here a grid-glued replica
method combined with SEM observation. This method allows histological staining
before dissolving the tissue and easy handling of replicas during immunogold labeling,
and keeps the whole replica surface intact without fragmentation. The procedure
described here is also useful for matched double-replica analysis allowing further
identification of labeled profiles in corresponding P-face and E-face.
acknowledged_ssus:
- _id: EM-Fac
acknowledgement: 'We thank Prof. Elek Molnár for providing us a pan-AMPAR anti-body
used in Fig.2 and Dr. Ludek Lovicar for technical assistance in scanning electron
microscope imaging. This work was supported by the European Union (HBP—Project Ref.
604102). '
alternative_title:
- Methods in Molecular Biology
article_processing_charge: No
author:
- first_name: Harumi
full_name: Harada, Harumi
id: 2E55CDF2-F248-11E8-B48F-1D18A9856A87
last_name: Harada
orcid: 0000-0001-7429-7896
- first_name: Ryuichi
full_name: Shigemoto, Ryuichi
id: 499F3ABC-F248-11E8-B48F-1D18A9856A87
last_name: Shigemoto
orcid: 0000-0001-8761-9444
citation:
ama: 'Harada H, Shigemoto R. Immunogold protein localization on grid-glued freeze-fracture
replicas. In: High-Resolution Imaging of Cellular Proteins. Vol 1474. Springer;
2016:203-216. doi:10.1007/978-1-4939-6352-2_12'
apa: Harada, H., & Shigemoto, R. (2016). Immunogold protein localization on
grid-glued freeze-fracture replicas. In High-Resolution Imaging of Cellular
Proteins (Vol. 1474, pp. 203–216). Springer. https://doi.org/10.1007/978-1-4939-6352-2_12
chicago: Harada, Harumi, and Ryuichi Shigemoto. “Immunogold Protein Localization
on Grid-Glued Freeze-Fracture Replicas.” In High-Resolution Imaging of Cellular
Proteins, 1474:203–16. Springer, 2016. https://doi.org/10.1007/978-1-4939-6352-2_12.
ieee: H. Harada and R. Shigemoto, “Immunogold protein localization on grid-glued
freeze-fracture replicas,” in High-Resolution Imaging of Cellular Proteins,
vol. 1474, Springer, 2016, pp. 203–216.
ista: 'Harada H, Shigemoto R. 2016.Immunogold protein localization on grid-glued
freeze-fracture replicas. In: High-Resolution Imaging of Cellular Proteins. Methods
in Molecular Biology, vol. 1474, 203–216.'
mla: Harada, Harumi, and Ryuichi Shigemoto. “Immunogold Protein Localization on
Grid-Glued Freeze-Fracture Replicas.” High-Resolution Imaging of Cellular Proteins,
vol. 1474, Springer, 2016, pp. 203–16, doi:10.1007/978-1-4939-6352-2_12.
short: H. Harada, R. Shigemoto, in:, High-Resolution Imaging of Cellular Proteins,
Springer, 2016, pp. 203–216.
date_created: 2018-12-11T11:50:06Z
date_published: 2016-08-12T00:00:00Z
date_updated: 2023-09-05T14:09:01Z
day: '12'
department:
- _id: RySh
doi: 10.1007/978-1-4939-6352-2_12
ec_funded: 1
intvolume: ' 1474'
language:
- iso: eng
month: '08'
oa_version: None
page: 203 - 216
project:
- _id: 25CD3DD2-B435-11E9-9278-68D0E5697425
call_identifier: FP7
grant_number: '604102'
name: Localization of ion channels and receptors by two and three-dimensional immunoelectron
microscopic approaches
publication: High-Resolution Imaging of Cellular Proteins
publication_identifier:
eissn:
- 1611-3349
issn:
- 0302-9743
publication_status: published
publisher: Springer
publist_id: '6281'
quality_controlled: '1'
status: public
title: Immunogold protein localization on grid-glued freeze-fracture replicas
type: book_chapter
user_id: c635000d-4b10-11ee-a964-aac5a93f6ac1
volume: 1474
year: '2016'
...
---
_id: '1278'
abstract:
- lang: eng
text: Adaptations of vestibulo-ocular and optokinetic response eye movements have
been studied as an experimental model of cerebellum-dependent motor learning.
Several previous physiological and pharmacological studies have consistently suggested
that the cerebellar flocculus (FL) Purkinje cells (P-cells) and the medial vestibular
nucleus (MVN) neurons targeted by FL (FL-targeted MVN neurons) may respectively
maintain the memory traces of short- and long-term adaptation. To study the basic
structures of the FL-MVN synapses by light microscopy (LM) and electron microscopy
(EM), we injected green florescence protein (GFP)-expressing lentivirus into FL
to anterogradely label the FL P-cell axons in C57BL/6J mice. The FL P-cell axonal
boutons were distributed in the magnocellular MVN and in the border region of
parvocellular MVN and prepositus hypoglossi (PrH). In the magnocellular MVN, the
FL-P cell axons mainly terminated on somata and proximal dendrites. On the other
hand, in the parvocellular MVN/PrH, the FL P-cell axonal synaptic boutons mainly
terminated on the relatively small-diameter (< 1 μm) distal dendrites of MVN
neurons, forming symmetrical synapses. The majority of such parvocellular MVN/PrH
neurons were determined to be glutamatergic by immunocytochemistry and in-situ
hybridization of GFP expressing transgenic mice. To further examine the spatial
relationship between the synapses of FL P-cells and those of vestibular nerve
on the neurons of the parvocellular MVN/ PrH, we added injections of biotinylated
dextran amine into the semicircular canal and anterogradely labeled vestibular
nerve axons in some mice. The MVN dendrites receiving the FL P-cell axonal synaptic
boutons often closely apposed vestibular nerve synaptic boutons in both LM and
EM studies. Such a partial overlap of synaptic boutons of FL P-cell axons with
those of vestibular nerve axons in the distal dendrites of MVN neurons suggests
that inhibitory synapses of FL P-cells may influence the function of neighboring
excitatory synapses of vestibular nerve in the parvocellular MVN/PrH neurons.
acknowledgement: This work was supported by RIKEN [to SN]; Grant-in-Aid from the Japan
Society for the Promotion of Science, https://www.jsps.go.jp/english/e-grants/ [22300112
to SN].
article_number: e0164037
article_processing_charge: No
article_type: original
author:
- first_name: Hitomi
full_name: Matsuno, Hitomi
last_name: Matsuno
- first_name: Moeko
full_name: Kudoh, Moeko
last_name: Kudoh
- first_name: Akiya
full_name: Watakabe, Akiya
last_name: Watakabe
- first_name: Tetsuo
full_name: Yamamori, Tetsuo
last_name: Yamamori
- first_name: Ryuichi
full_name: Shigemoto, Ryuichi
id: 499F3ABC-F248-11E8-B48F-1D18A9856A87
last_name: Shigemoto
orcid: 0000-0001-8761-9444
- first_name: Soichi
full_name: Nagao, Soichi
last_name: Nagao
citation:
ama: 'Matsuno H, Kudoh M, Watakabe A, Yamamori T, Shigemoto R, Nagao S. Distribution
and structure of synapses on medial vestibular nuclear neurons targeted by cerebellar
flocculus purkinje cells and vestibular nerve in mice: Light and electron microscopy
studies. PLoS One. 2016;11(10). doi:10.1371/journal.pone.0164037'
apa: 'Matsuno, H., Kudoh, M., Watakabe, A., Yamamori, T., Shigemoto, R., & Nagao,
S. (2016). Distribution and structure of synapses on medial vestibular nuclear
neurons targeted by cerebellar flocculus purkinje cells and vestibular nerve in
mice: Light and electron microscopy studies. PLoS One. Public Library of
Science. https://doi.org/10.1371/journal.pone.0164037'
chicago: 'Matsuno, Hitomi, Moeko Kudoh, Akiya Watakabe, Tetsuo Yamamori, Ryuichi
Shigemoto, and Soichi Nagao. “Distribution and Structure of Synapses on Medial
Vestibular Nuclear Neurons Targeted by Cerebellar Flocculus Purkinje Cells and
Vestibular Nerve in Mice: Light and Electron Microscopy Studies.” PLoS One.
Public Library of Science, 2016. https://doi.org/10.1371/journal.pone.0164037.'
ieee: 'H. Matsuno, M. Kudoh, A. Watakabe, T. Yamamori, R. Shigemoto, and S. Nagao,
“Distribution and structure of synapses on medial vestibular nuclear neurons targeted
by cerebellar flocculus purkinje cells and vestibular nerve in mice: Light and
electron microscopy studies,” PLoS One, vol. 11, no. 10. Public Library
of Science, 2016.'
ista: 'Matsuno H, Kudoh M, Watakabe A, Yamamori T, Shigemoto R, Nagao S. 2016. Distribution
and structure of synapses on medial vestibular nuclear neurons targeted by cerebellar
flocculus purkinje cells and vestibular nerve in mice: Light and electron microscopy
studies. PLoS One. 11(10), e0164037.'
mla: 'Matsuno, Hitomi, et al. “Distribution and Structure of Synapses on Medial
Vestibular Nuclear Neurons Targeted by Cerebellar Flocculus Purkinje Cells and
Vestibular Nerve in Mice: Light and Electron Microscopy Studies.” PLoS One,
vol. 11, no. 10, e0164037, Public Library of Science, 2016, doi:10.1371/journal.pone.0164037.'
short: H. Matsuno, M. Kudoh, A. Watakabe, T. Yamamori, R. Shigemoto, S. Nagao, PLoS
One 11 (2016).
date_created: 2018-12-11T11:51:06Z
date_published: 2016-10-06T00:00:00Z
date_updated: 2021-01-12T06:49:34Z
day: '06'
ddc:
- '570'
- '571'
department:
- _id: RySh
doi: 10.1371/journal.pone.0164037
file:
- access_level: open_access
checksum: 7c0ba0ca6d79844059158059d2a38d25
content_type: application/pdf
creator: system
date_created: 2018-12-12T10:17:16Z
date_updated: 2020-07-14T12:44:42Z
file_id: '5269'
file_name: IST-2016-689-v1+1_journal.pone.0164037.PDF
file_size: 3657084
relation: main_file
file_date_updated: 2020-07-14T12:44:42Z
has_accepted_license: '1'
intvolume: ' 11'
issue: '10'
language:
- iso: eng
month: '10'
oa: 1
oa_version: Published Version
publication: PLoS One
publication_status: published
publisher: Public Library of Science
publist_id: '6038'
pubrep_id: '689'
quality_controlled: '1'
scopus_import: 1
status: public
title: 'Distribution and structure of synapses on medial vestibular nuclear neurons
targeted by cerebellar flocculus purkinje cells and vestibular nerve in mice: Light
and electron microscopy studies'
tmp:
image: /images/cc_by.png
legal_code_url: https://creativecommons.org/licenses/by/4.0/legalcode
name: Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)
short: CC BY (4.0)
type: journal_article
user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87
volume: 11
year: '2016'
...
---
_id: '1546'
abstract:
- lang: eng
text: Synaptic efficacy and precision are influenced by the coupling of voltage-gated
Ca2+ channels (VGCCs) to vesicles. But because the topography of VGCCs and their
proximity to vesicles is unknown, a quantitative understanding of the determinants
of vesicular release at nanometer scale is lacking. To investigate this, we combined
freeze-fracture replica immunogold labeling of Cav2.1 channels, local [Ca2+] imaging,
and patch pipette perfusion of EGTA at the calyx of Held. Between postnatal day
7 and 21, VGCCs formed variable sized clusters and vesicular release became less
sensitive to EGTA, whereas fixed Ca2+ buffer properties remained constant. Experimentally
constrained reaction-diffusion simulations suggest that Ca2+ sensors for vesicular
release are located at the perimeter of VGCC clusters (<30nm) and predict that
VGCC number per cluster determines vesicular release probability without altering
release time course. This "perimeter release model" provides a unifying
framework accounting for developmental changes in both synaptic efficacy and time
course.
acknowledgement: This work was supported by the Core Research for Evolutional Science
and Technology (CREST) of Japan Science and Technology Agency to T.T. and R.S.;
by the funding provided by Okinawa Institute of Science and Technology (OIST) to
T.T. and Y.N.; by JSPS Core-to-Core Program, A. Advanced Networks to T.T.; by the
Grant-in-Aid for Young Scientists from the Japanese Ministry of Education, Culture,
Sports, Science and Technology (#23700474) to Y.N.; by the Centre National de la
Recherche Scientifique through the Actions Thematiques et Initatives sur Programme,
Fondation Fyssen, Fondation pour la Recherche Medicale, Federation pour la Recherche
sur le Cerveau, Agence Nationale de la Recherche (ANR-2007-Neuro-008-01 and ANR-2010-BLAN-1411-01)
to D.D. and Y.N.; and by the European Commission Coordination Action ENINET (LSHM-CT-2005-19063)
to D.D. and R.A.S. R.A.S. and J.S.R. were funded by Wellcome Trust Senior (064413)
and Principal (095667) Research Fellowship and an ERC advance grant (294667) to
RAS.
author:
- first_name: Yukihiro
full_name: Nakamura, Yukihiro
last_name: Nakamura
- first_name: Harumi
full_name: Harada, Harumi
id: 2E55CDF2-F248-11E8-B48F-1D18A9856A87
last_name: Harada
orcid: 0000-0001-7429-7896
- first_name: Naomi
full_name: Kamasawa, Naomi
last_name: Kamasawa
- first_name: Ko
full_name: Matsui, Ko
last_name: Matsui
- first_name: Jason
full_name: Rothman, Jason
last_name: Rothman
- first_name: Ryuichi
full_name: Shigemoto, Ryuichi
id: 499F3ABC-F248-11E8-B48F-1D18A9856A87
last_name: Shigemoto
orcid: 0000-0001-8761-9444
- first_name: R Angus
full_name: Silver, R Angus
last_name: Silver
- first_name: David
full_name: Digregorio, David
last_name: Digregorio
- first_name: Tomoyuki
full_name: Takahashi, Tomoyuki
last_name: Takahashi
citation:
ama: Nakamura Y, Harada H, Kamasawa N, et al. Nanoscale distribution of presynaptic
Ca2+ channels and its impact on vesicular release during development. Neuron.
2015;85(1):145-158. doi:10.1016/j.neuron.2014.11.019
apa: Nakamura, Y., Harada, H., Kamasawa, N., Matsui, K., Rothman, J., Shigemoto,
R., … Takahashi, T. (2015). Nanoscale distribution of presynaptic Ca2+ channels
and its impact on vesicular release during development. Neuron. Elsevier.
https://doi.org/10.1016/j.neuron.2014.11.019
chicago: Nakamura, Yukihiro, Harumi Harada, Naomi Kamasawa, Ko Matsui, Jason Rothman,
Ryuichi Shigemoto, R Angus Silver, David Digregorio, and Tomoyuki Takahashi. “Nanoscale
Distribution of Presynaptic Ca2+ Channels and Its Impact on Vesicular Release
during Development.” Neuron. Elsevier, 2015. https://doi.org/10.1016/j.neuron.2014.11.019.
ieee: Y. Nakamura et al., “Nanoscale distribution of presynaptic Ca2+ channels
and its impact on vesicular release during development,” Neuron, vol. 85,
no. 1. Elsevier, pp. 145–158, 2015.
ista: Nakamura Y, Harada H, Kamasawa N, Matsui K, Rothman J, Shigemoto R, Silver
RA, Digregorio D, Takahashi T. 2015. Nanoscale distribution of presynaptic Ca2+
channels and its impact on vesicular release during development. Neuron. 85(1),
145–158.
mla: Nakamura, Yukihiro, et al. “Nanoscale Distribution of Presynaptic Ca2+ Channels
and Its Impact on Vesicular Release during Development.” Neuron, vol. 85,
no. 1, Elsevier, 2015, pp. 145–58, doi:10.1016/j.neuron.2014.11.019.
short: Y. Nakamura, H. Harada, N. Kamasawa, K. Matsui, J. Rothman, R. Shigemoto,
R.A. Silver, D. Digregorio, T. Takahashi, Neuron 85 (2015) 145–158.
date_created: 2018-12-11T11:52:39Z
date_published: 2015-01-07T00:00:00Z
date_updated: 2021-01-12T06:51:31Z
day: '07'
ddc:
- '570'
department:
- _id: RySh
doi: 10.1016/j.neuron.2014.11.019
file:
- access_level: open_access
checksum: 725f4d5be2dbb44b283ce722645ef37d
content_type: application/pdf
creator: system
date_created: 2018-12-12T10:15:47Z
date_updated: 2020-07-14T12:45:01Z
file_id: '5170'
file_name: IST-2016-482-v1+1_1-s2.0-S0896627314010472-main.pdf
file_size: 3080111
relation: main_file
file_date_updated: 2020-07-14T12:45:01Z
has_accepted_license: '1'
intvolume: ' 85'
issue: '1'
language:
- iso: eng
month: '01'
oa: 1
oa_version: Published Version
page: 145 - 158
publication: Neuron
publication_status: published
publisher: Elsevier
publist_id: '5625'
pubrep_id: '482'
quality_controlled: '1'
scopus_import: 1
status: public
title: Nanoscale distribution of presynaptic Ca2+ channels and its impact on vesicular
release during development
tmp:
image: /images/cc_by.png
legal_code_url: https://creativecommons.org/licenses/by/4.0/legalcode
name: Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)
short: CC BY (4.0)
type: journal_article
user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87
volume: 85
year: '2015'
...
---
_id: '1557'
abstract:
- lang: eng
text: γ-Aminobutyric acid (GABA)- and glycine-mediated hyperpolarizing inhibition
is associated with a chloride influx that depends on the inwardly directed chloride
electrochemical gradient. In neurons, the extrusion of chloride from the cytosol
primarily depends on the expression of an isoform of potassium-chloride cotransporters
(KCC2s). KCC2 is crucial in the regulation of the inhibitory tone of neural circuits,
including pain processing neural assemblies. Thus we investigated the cellular
distribution of KCC2 in neurons underlying pain processing in the superficial
spinal dorsal horn of rats by using high-resolution immunocytochemical methods.
We demonstrated that perikarya and dendrites widely expressed KCC2, but axon terminals
proved to be negative for KCC2. In single ultrathin sections, silver deposits
labeling KCC2 molecules showed different densities on the surface of dendritic
profiles, some of which were negative for KCC2. In freeze fracture replicas and
tissue sections double stained for the β3-subunit of GABAA receptors and KCC2,
GABAA receptors were revealed on dendritic segments with high and also with low
KCC2 densities. By measuring the distances between spots immunoreactive for gephyrin
(a scaffolding protein of GABAA and glycine receptors) and KCC2 on the surface
of neurokinin 1 (NK1) receptor-immunoreactive dendrites, we found that gephyrin-immunoreactive
spots were located at various distances from KCC2 cotransporters; 5.7 % of them
were recovered in the middle of 4-10-μm-long dendritic segments that were free
of KCC2 immunostaining. The variable local densities of KCC2 may result in variable
postsynaptic potentials evoked by the activation of GABAA and glycine receptors
along the dendrites of spinal neurons.
acknowledgement: "Funded by:\r\nHungarian Academy of Sciences. Grant Number: MTA-TKI
242\r\nHungarian Brain Research Program. Grant Number: KTIA_NAP_13-1-2013-0001\r\nSolution
Oriented Research for Science and Technology from the Japan Science and Technology
Agency Japanese Ministry of Education, Culture, Sports, Science and Technology"
author:
- first_name: Fariba
full_name: Javdani, Fariba
last_name: Javdani
- first_name: Krisztina
full_name: Holló, Krisztina
last_name: Holló
- first_name: Krisztina
full_name: Hegedűs, Krisztina
last_name: Hegedűs
- first_name: Gréta
full_name: Kis, Gréta
last_name: Kis
- first_name: Zoltán
full_name: Hegyi, Zoltán
last_name: Hegyi
- first_name: Klaudia
full_name: Dócs, Klaudia
last_name: Dócs
- first_name: Yu
full_name: Kasugai, Yu
last_name: Kasugai
- first_name: Yugo
full_name: Fukazawa, Yugo
last_name: Fukazawa
- first_name: Ryuichi
full_name: Shigemoto, Ryuichi
id: 499F3ABC-F248-11E8-B48F-1D18A9856A87
last_name: Shigemoto
orcid: 0000-0001-8761-9444
- first_name: Miklós
full_name: Antal, Miklós
last_name: Antal
citation:
ama: Javdani F, Holló K, Hegedűs K, et al. Differential expression patterns of K+Cl-
cotransporter 2 in neurons within the superficial spinal dorsal horn of rats.
Journal of Comparative Neurology. 2015;523(13):1967-1983. doi:10.1002/cne.23774
apa: Javdani, F., Holló, K., Hegedűs, K., Kis, G., Hegyi, Z., Dócs, K., … Antal,
M. (2015). Differential expression patterns of K+Cl- cotransporter 2 in neurons
within the superficial spinal dorsal horn of rats. Journal of Comparative Neurology.
Wiley-Blackwell. https://doi.org/10.1002/cne.23774
chicago: Javdani, Fariba, Krisztina Holló, Krisztina Hegedűs, Gréta Kis, Zoltán
Hegyi, Klaudia Dócs, Yu Kasugai, Yugo Fukazawa, Ryuichi Shigemoto, and Miklós
Antal. “Differential Expression Patterns of K+Cl- Cotransporter 2 in Neurons within
the Superficial Spinal Dorsal Horn of Rats.” Journal of Comparative Neurology.
Wiley-Blackwell, 2015. https://doi.org/10.1002/cne.23774.
ieee: F. Javdani et al., “Differential expression patterns of K+Cl- cotransporter
2 in neurons within the superficial spinal dorsal horn of rats,” Journal of
Comparative Neurology, vol. 523, no. 13. Wiley-Blackwell, pp. 1967–1983, 2015.
ista: Javdani F, Holló K, Hegedűs K, Kis G, Hegyi Z, Dócs K, Kasugai Y, Fukazawa
Y, Shigemoto R, Antal M. 2015. Differential expression patterns of K+Cl- cotransporter
2 in neurons within the superficial spinal dorsal horn of rats. Journal of Comparative
Neurology. 523(13), 1967–1983.
mla: Javdani, Fariba, et al. “Differential Expression Patterns of K+Cl- Cotransporter
2 in Neurons within the Superficial Spinal Dorsal Horn of Rats.” Journal of
Comparative Neurology, vol. 523, no. 13, Wiley-Blackwell, 2015, pp. 1967–83,
doi:10.1002/cne.23774.
short: F. Javdani, K. Holló, K. Hegedűs, G. Kis, Z. Hegyi, K. Dócs, Y. Kasugai,
Y. Fukazawa, R. Shigemoto, M. Antal, Journal of Comparative Neurology 523 (2015)
1967–1983.
date_created: 2018-12-11T11:52:42Z
date_published: 2015-09-01T00:00:00Z
date_updated: 2021-01-12T06:51:35Z
day: '01'
department:
- _id: RySh
doi: 10.1002/cne.23774
intvolume: ' 523'
issue: '13'
language:
- iso: eng
month: '09'
oa_version: None
page: 1967 - 1983
publication: Journal of Comparative Neurology
publication_status: published
publisher: Wiley-Blackwell
publist_id: '5614'
quality_controlled: '1'
scopus_import: 1
status: public
title: Differential expression patterns of K+Cl- cotransporter 2 in neurons within
the superficial spinal dorsal horn of rats
type: journal_article
user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87
volume: 523
year: '2015'
...
---
_id: '1895'
abstract:
- lang: eng
text: Major histocompatibility complex class I (MHCI) molecules were recently identified
as novel regulators of synaptic plasticity. These molecules are expressed in various
brain areas, especially in regions undergoing activity-dependent synaptic plasticity,
but their role in the nucleus accumbens (NAc) is unknown. In this study, we investigated
the effects of genetic disruption of MHCI function, through deletion of β2-microblobulin,
which causes lack of cell surface expression of MHCI. First, we confirmed that
MHCI molecules are expressed in the NAc core in wild-type mice. Second, we performed
electrophysiological recordings with NAc core slices from wild-type and β2-microglobulin
knock-out mice lacking cell surface expression of MHCI. We found that low frequency
stimulation induced long-term depression in wild-type but not knock-out mice,
whereas high frequency stimulation induced long-term potentiation in both genotypes,
with a larger magnitude in knock-out mice. Furthermore, we demonstrated that knock-out
mice showed more persistent behavioral sensitization to cocaine, which is a NAc-related
behavior. Using this model, we analyzed the density of total AMPA receptors and
their subunits GluR1 and GluR2 in the NAc core, by SDS-digested freeze-fracture
replica labeling. After repeated cocaine exposure, the density of GluR1 was increased,
but there was no change in total AMPA receptors and GluR2 levels in wildtype mice.
In contrast, following repeated cocaine exposure, increased densities of total
AMPA receptors, GluR1 and GluR2 were observed in knock-out mice. These results
indicate that functional deficiency of MHCI enhances synaptic potentiation, induced
by electrical and pharmacological stimulation.
acknowledgement: This work was supported in part by a Grant-in-Aid for Scientific
Research on Innovative Areas (Comprehensive Brain Science Network) and (B) 17330153,
from the Ministry of Education, Culture, Sports, Science and Technology of Japan.
article_number: e107099
author:
- first_name: Mitsuhiro
full_name: Edamura, Mitsuhiro
last_name: Edamura
- first_name: Gen
full_name: Murakami, Gen
last_name: Murakami
- first_name: Hongrui
full_name: Meng, Hongrui
last_name: Meng
- first_name: Makoto
full_name: Itakura, Makoto
last_name: Itakura
- first_name: Ryuichi
full_name: Shigemoto, Ryuichi
id: 499F3ABC-F248-11E8-B48F-1D18A9856A87
last_name: Shigemoto
orcid: 0000-0001-8761-9444
- first_name: Atsuo
full_name: Fukuda, Atsuo
last_name: Fukuda
- first_name: Daiichiro
full_name: Nakahara, Daiichiro
last_name: Nakahara
citation:
ama: Edamura M, Murakami G, Meng H, et al. Functional deficiency of MHC class i
enhances LTP and abolishes LTD in the nucleus accumbens of mice. PLoS One.
2014;9(9). doi:10.1371/journal.pone.0107099
apa: Edamura, M., Murakami, G., Meng, H., Itakura, M., Shigemoto, R., Fukuda, A.,
& Nakahara, D. (2014). Functional deficiency of MHC class i enhances LTP and
abolishes LTD in the nucleus accumbens of mice. PLoS One. Public Library
of Science. https://doi.org/10.1371/journal.pone.0107099
chicago: Edamura, Mitsuhiro, Gen Murakami, Hongrui Meng, Makoto Itakura, Ryuichi
Shigemoto, Atsuo Fukuda, and Daiichiro Nakahara. “Functional Deficiency of MHC
Class i Enhances LTP and Abolishes LTD in the Nucleus Accumbens of Mice.” PLoS
One. Public Library of Science, 2014. https://doi.org/10.1371/journal.pone.0107099.
ieee: M. Edamura et al., “Functional deficiency of MHC class i enhances LTP
and abolishes LTD in the nucleus accumbens of mice,” PLoS One, vol. 9,
no. 9. Public Library of Science, 2014.
ista: Edamura M, Murakami G, Meng H, Itakura M, Shigemoto R, Fukuda A, Nakahara
D. 2014. Functional deficiency of MHC class i enhances LTP and abolishes LTD in
the nucleus accumbens of mice. PLoS One. 9(9), e107099.
mla: Edamura, Mitsuhiro, et al. “Functional Deficiency of MHC Class i Enhances LTP
and Abolishes LTD in the Nucleus Accumbens of Mice.” PLoS One, vol. 9,
no. 9, e107099, Public Library of Science, 2014, doi:10.1371/journal.pone.0107099.
short: M. Edamura, G. Murakami, H. Meng, M. Itakura, R. Shigemoto, A. Fukuda, D.
Nakahara, PLoS One 9 (2014).
date_created: 2018-12-11T11:54:35Z
date_published: 2014-09-30T00:00:00Z
date_updated: 2021-01-12T06:53:54Z
day: '30'
ddc:
- '570'
department:
- _id: RySh
doi: 10.1371/journal.pone.0107099
file:
- access_level: open_access
checksum: 1f3be936be93114596d61ba44cacee69
content_type: application/pdf
creator: system
date_created: 2018-12-12T10:09:01Z
date_updated: 2020-07-14T12:45:20Z
file_id: '4724'
file_name: IST-2016-439-v1+1_journal.pone.0107099.pdf
file_size: 6262085
relation: main_file
file_date_updated: 2020-07-14T12:45:20Z
has_accepted_license: '1'
intvolume: ' 9'
issue: '9'
language:
- iso: eng
month: '09'
oa: 1
oa_version: Published Version
publication: PLoS One
publication_status: published
publisher: Public Library of Science
publist_id: '5200'
pubrep_id: '439'
scopus_import: 1
status: public
title: Functional deficiency of MHC class i enhances LTP and abolishes LTD in the
nucleus accumbens of mice
tmp:
image: /images/cc_by.png
legal_code_url: https://creativecommons.org/licenses/by/4.0/legalcode
name: Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)
short: CC BY (4.0)
type: journal_article
user_id: 4435EBFC-F248-11E8-B48F-1D18A9856A87
volume: 9
year: '2014'
...
---
_id: '1898'
abstract:
- lang: eng
text: Fast synaptic transmission is important for rapid information processing.
To explore the maximal rate of neuronal signaling and to analyze the presynaptic
mechanisms, we focused on the input layer of the cerebellar cortex, where exceptionally
high action potential (AP) frequencies have been reported invivo. With paired
recordings between presynaptic cerebellar mossy fiber boutons and postsynaptic
granule cells, we demonstrate reliable neurotransmission upto ~1 kHz. Presynaptic
APs are ultrafast, with ~100μs half-duration. Both Kv1 and Kv3 potassium channels
mediate the fast repolarization, rapidly inactivating sodium channels ensure metabolic
efficiency, and little AP broadening occurs during bursts of up to 1.5 kHz. Presynaptic
Cav2.1 (P/Q-type) calcium channels open efficiently during ultrafast APs. Furthermore,
a subset of synaptic vesicles is tightly coupled to Ca2+ channels, and vesicles
are rapidly recruited to the release site. These data reveal mechanisms of presynaptic
AP generation and transmitter release underlying neuronal kHz signaling.
author:
- first_name: Andreas
full_name: Ritzau Jost, Andreas
last_name: Ritzau Jost
- first_name: Igor
full_name: Delvendahl, Igor
last_name: Delvendahl
- first_name: Annika
full_name: Rings, Annika
last_name: Rings
- first_name: Niklas
full_name: Byczkowicz, Niklas
last_name: Byczkowicz
- first_name: Harumi
full_name: Harada, Harumi
id: 2E55CDF2-F248-11E8-B48F-1D18A9856A87
last_name: Harada
orcid: 0000-0001-7429-7896
- first_name: Ryuichi
full_name: Shigemoto, Ryuichi
id: 499F3ABC-F248-11E8-B48F-1D18A9856A87
last_name: Shigemoto
orcid: 0000-0001-8761-9444
- first_name: Johannes
full_name: Hirrlinger, Johannes
last_name: Hirrlinger
- first_name: Jens
full_name: Eilers, Jens
last_name: Eilers
- first_name: Stefan
full_name: Hallermann, Stefan
last_name: Hallermann
citation:
ama: Ritzau Jost A, Delvendahl I, Rings A, et al. Ultrafast action potentials mediate
kilohertz signaling at a central synapse. Neuron. 2014;84(1):152-163. doi:10.1016/j.neuron.2014.08.036
apa: Ritzau Jost, A., Delvendahl, I., Rings, A., Byczkowicz, N., Harada, H., Shigemoto,
R., … Hallermann, S. (2014). Ultrafast action potentials mediate kilohertz signaling
at a central synapse. Neuron. Elsevier. https://doi.org/10.1016/j.neuron.2014.08.036
chicago: Ritzau Jost, Andreas, Igor Delvendahl, Annika Rings, Niklas Byczkowicz,
Harumi Harada, Ryuichi Shigemoto, Johannes Hirrlinger, Jens Eilers, and Stefan
Hallermann. “Ultrafast Action Potentials Mediate Kilohertz Signaling at a Central
Synapse.” Neuron. Elsevier, 2014. https://doi.org/10.1016/j.neuron.2014.08.036.
ieee: A. Ritzau Jost et al., “Ultrafast action potentials mediate kilohertz
signaling at a central synapse,” Neuron, vol. 84, no. 1. Elsevier, pp.
152–163, 2014.
ista: Ritzau Jost A, Delvendahl I, Rings A, Byczkowicz N, Harada H, Shigemoto R,
Hirrlinger J, Eilers J, Hallermann S. 2014. Ultrafast action potentials mediate
kilohertz signaling at a central synapse. Neuron. 84(1), 152–163.
mla: Ritzau Jost, Andreas, et al. “Ultrafast Action Potentials Mediate Kilohertz
Signaling at a Central Synapse.” Neuron, vol. 84, no. 1, Elsevier, 2014,
pp. 152–63, doi:10.1016/j.neuron.2014.08.036.
short: A. Ritzau Jost, I. Delvendahl, A. Rings, N. Byczkowicz, H. Harada, R. Shigemoto,
J. Hirrlinger, J. Eilers, S. Hallermann, Neuron 84 (2014) 152–163.
date_created: 2018-12-11T11:54:36Z
date_published: 2014-10-01T00:00:00Z
date_updated: 2021-01-12T06:53:55Z
day: '01'
department:
- _id: RySh
doi: 10.1016/j.neuron.2014.08.036
intvolume: ' 84'
issue: '1'
language:
- iso: eng
month: '10'
oa_version: None
page: 152 - 163
publication: Neuron
publication_status: published
publisher: Elsevier
publist_id: '5197'
quality_controlled: '1'
scopus_import: 1
status: public
title: Ultrafast action potentials mediate kilohertz signaling at a central synapse
type: journal_article
user_id: 4435EBFC-F248-11E8-B48F-1D18A9856A87
volume: 84
year: '2014'
...