---
_id: '2164'
abstract:
- lang: eng
  text: 'Neuronal ectopia, such as granule cell dispersion (GCD) in temporal lobe
    epilepsy (TLE), has been assumed to result from a migration defect during development.
    Indeed, recent studies reported that aberrant migration of neonatal-generated
    dentate granule cells (GCs) increased the risk to develop epilepsy later in life.
    On the contrary, in the present study, we show that fully differentiated GCs become
    motile following the induction of epileptiform activity, resulting in GCD. Hippocampal
    slice cultures from transgenic mice expressing green fluorescent protein in differentiated,
    but not in newly generated GCs, were incubated with the glutamate receptor agonist
    kainate (KA), which induced GC burst activity and GCD. Using real-time microscopy,
    we observed that KA-exposed, differentiated GCs translocated their cell bodies
    and changed their dendritic organization. As found in human TLE, KA application
    was associated with decreased expression of the extracellular matrix protein Reelin,
    particularly in hilar interneurons. Together these findings suggest that KA-induced
    motility of differentiated GCs contributes to the development of GCD and establish
    slice cultures as a model to study neuronal changes induced by epileptiform activity. '
author:
- first_name: Xuejun
  full_name: Chai, Xuejun
  last_name: Chai
- first_name: Gert
  full_name: Münzner, Gert
  last_name: Münzner
- first_name: Shanting
  full_name: Zhao, Shanting
  last_name: Zhao
- first_name: Stefanie
  full_name: Tinnes, Stefanie
  last_name: Tinnes
- first_name: Janina
  full_name: Kowalski, Janina
  id: 3F3CA136-F248-11E8-B48F-1D18A9856A87
  last_name: Kowalski
- first_name: Ute
  full_name: Häussler, Ute
  last_name: Häussler
- first_name: Christina
  full_name: Young, Christina
  last_name: Young
- first_name: Carola
  full_name: Haas, Carola
  last_name: Haas
- first_name: Michael
  full_name: Frotscher, Michael
  last_name: Frotscher
citation:
  ama: Chai X, Münzner G, Zhao S, et al. Epilepsy-induced motility of differentiated
    neurons. <i>Cerebral Cortex</i>. 2014;24(8):2130-2140. doi:<a href="https://doi.org/10.1093/cercor/bht067">10.1093/cercor/bht067</a>
  apa: Chai, X., Münzner, G., Zhao, S., Tinnes, S., Kowalski, J., Häussler, U., …
    Frotscher, M. (2014). Epilepsy-induced motility of differentiated neurons. <i>Cerebral
    Cortex</i>. Oxford University Press. <a href="https://doi.org/10.1093/cercor/bht067">https://doi.org/10.1093/cercor/bht067</a>
  chicago: Chai, Xuejun, Gert Münzner, Shanting Zhao, Stefanie Tinnes, Janina Kowalski,
    Ute Häussler, Christina Young, Carola Haas, and Michael Frotscher. “Epilepsy-Induced
    Motility of Differentiated Neurons.” <i>Cerebral Cortex</i>. Oxford University
    Press, 2014. <a href="https://doi.org/10.1093/cercor/bht067">https://doi.org/10.1093/cercor/bht067</a>.
  ieee: X. Chai <i>et al.</i>, “Epilepsy-induced motility of differentiated neurons,”
    <i>Cerebral Cortex</i>, vol. 24, no. 8. Oxford University Press, pp. 2130–2140,
    2014.
  ista: Chai X, Münzner G, Zhao S, Tinnes S, Kowalski J, Häussler U, Young C, Haas
    C, Frotscher M. 2014. Epilepsy-induced motility of differentiated neurons. Cerebral
    Cortex. 24(8), 2130–2140.
  mla: Chai, Xuejun, et al. “Epilepsy-Induced Motility of Differentiated Neurons.”
    <i>Cerebral Cortex</i>, vol. 24, no. 8, Oxford University Press, 2014, pp. 2130–40,
    doi:<a href="https://doi.org/10.1093/cercor/bht067">10.1093/cercor/bht067</a>.
  short: X. Chai, G. Münzner, S. Zhao, S. Tinnes, J. Kowalski, U. Häussler, C. Young,
    C. Haas, M. Frotscher, Cerebral Cortex 24 (2014) 2130–2140.
date_created: 2018-12-11T11:56:04Z
date_published: 2014-08-01T00:00:00Z
date_updated: 2021-01-12T06:55:43Z
day: '01'
department:
- _id: PeJo
doi: 10.1093/cercor/bht067
intvolume: '        24'
issue: '8'
language:
- iso: eng
month: '08'
oa_version: None
page: 2130 - 2140
publication: Cerebral Cortex
publication_status: published
publisher: Oxford University Press
publist_id: '4820'
quality_controlled: '1'
scopus_import: 1
status: public
title: Epilepsy-induced motility of differentiated neurons
type: journal_article
user_id: 4435EBFC-F248-11E8-B48F-1D18A9856A87
volume: 24
year: '2014'
...
---
_id: '2176'
abstract:
- lang: eng
  text: Electron microscopy (EM) allows for the simultaneous visualization of all
    tissue components at high resolution. However, the extent to which conventional
    aldehyde fixation and ethanol dehydration of the tissue alter the fine structure
    of cells and organelles, thereby preventing detection of subtle structural changes
    induced by an experiment, has remained an issue. Attempts have been made to rapidly
    freeze tissue to preserve native ultrastructure. Shock-freezing of living tissue
    under high pressure (high-pressure freezing, HPF) followed by cryosubstitution
    of the tissue water avoids aldehyde fixation and dehydration in ethanol; the tissue
    water is immobilized in â ̂1/450 ms, and a close-to-native fine structure of cells,
    organelles and molecules is preserved. Here we describe a protocol for HPF that
    is useful to monitor ultrastructural changes associated with functional changes
    at synapses in the brain but can be applied to many other tissues as well. The
    procedure requires a high-pressure freezer and takes a minimum of 7 d but can
    be paused at several points.
author:
- first_name: Daniel
  full_name: Studer, Daniel
  last_name: Studer
- first_name: Shanting
  full_name: Zhao, Shanting
  last_name: Zhao
- first_name: Xuejun
  full_name: Chai, Xuejun
  last_name: Chai
- first_name: Peter M
  full_name: Jonas, Peter M
  id: 353C1B58-F248-11E8-B48F-1D18A9856A87
  last_name: Jonas
  orcid: 0000-0001-5001-4804
- first_name: Werner
  full_name: Graber, Werner
  last_name: Graber
- first_name: Sigrun
  full_name: Nestel, Sigrun
  last_name: Nestel
- first_name: Michael
  full_name: Frotscher, Michael
  last_name: Frotscher
citation:
  ama: Studer D, Zhao S, Chai X, et al. Capture of activity-induced ultrastructural
    changes at synapses by high-pressure freezing of brain tissue. <i>Nature Protocols</i>.
    2014;9(6):1480-1495. doi:<a href="https://doi.org/10.1038/nprot.2014.099">10.1038/nprot.2014.099</a>
  apa: Studer, D., Zhao, S., Chai, X., Jonas, P. M., Graber, W., Nestel, S., &#38;
    Frotscher, M. (2014). Capture of activity-induced ultrastructural changes at synapses
    by high-pressure freezing of brain tissue. <i>Nature Protocols</i>. Nature Publishing
    Group. <a href="https://doi.org/10.1038/nprot.2014.099">https://doi.org/10.1038/nprot.2014.099</a>
  chicago: Studer, Daniel, Shanting Zhao, Xuejun Chai, Peter M Jonas, Werner Graber,
    Sigrun Nestel, and Michael Frotscher. “Capture of Activity-Induced Ultrastructural
    Changes at Synapses by High-Pressure Freezing of Brain Tissue.” <i>Nature Protocols</i>.
    Nature Publishing Group, 2014. <a href="https://doi.org/10.1038/nprot.2014.099">https://doi.org/10.1038/nprot.2014.099</a>.
  ieee: D. Studer <i>et al.</i>, “Capture of activity-induced ultrastructural changes
    at synapses by high-pressure freezing of brain tissue,” <i>Nature Protocols</i>,
    vol. 9, no. 6. Nature Publishing Group, pp. 1480–1495, 2014.
  ista: Studer D, Zhao S, Chai X, Jonas PM, Graber W, Nestel S, Frotscher M. 2014.
    Capture of activity-induced ultrastructural changes at synapses by high-pressure
    freezing of brain tissue. Nature Protocols. 9(6), 1480–1495.
  mla: Studer, Daniel, et al. “Capture of Activity-Induced Ultrastructural Changes
    at Synapses by High-Pressure Freezing of Brain Tissue.” <i>Nature Protocols</i>,
    vol. 9, no. 6, Nature Publishing Group, 2014, pp. 1480–95, doi:<a href="https://doi.org/10.1038/nprot.2014.099">10.1038/nprot.2014.099</a>.
  short: D. Studer, S. Zhao, X. Chai, P.M. Jonas, W. Graber, S. Nestel, M. Frotscher,
    Nature Protocols 9 (2014) 1480–1495.
date_created: 2018-12-11T11:56:09Z
date_published: 2014-05-29T00:00:00Z
date_updated: 2021-01-12T06:55:47Z
day: '29'
department:
- _id: PeJo
doi: 10.1038/nprot.2014.099
intvolume: '         9'
issue: '6'
language:
- iso: eng
month: '05'
oa_version: None
page: 1480 - 1495
project:
- _id: 25BDE9A4-B435-11E9-9278-68D0E5697425
  grant_number: SFB-TR3-TP10B
  name: Glutamaterge synaptische Übertragung und Plastizität in hippocampalen Mikroschaltkreisen
publication: Nature Protocols
publication_status: published
publisher: Nature Publishing Group
publist_id: '4807'
quality_controlled: '1'
scopus_import: 1
status: public
title: Capture of activity-induced ultrastructural changes at synapses by high-pressure
  freezing of brain tissue
type: journal_article
user_id: 4435EBFC-F248-11E8-B48F-1D18A9856A87
volume: 9
year: '2014'
...
---
_id: '2228'
abstract:
- lang: eng
  text: Fast-spiking, parvalbumin-expressing GABAergic interneurons, a large proportion
    of which are basket cells (BCs), have a key role in feedforward and feedback inhibition,
    gamma oscillations and complex information processing. For these functions, fast
    propagation of action potentials (APs) from the soma to the presynaptic terminals
    is important. However, the functional properties of interneuron axons remain elusive.
    We examined interneuron axons by confocally targeted subcellular patch-clamp recording
    in rat hippocampal slices. APs were initiated in the proximal axon ∼20 μm from
    the soma and propagated to the distal axon with high reliability and speed. Subcellular
    mapping revealed a stepwise increase of Na^+ conductance density from the soma
    to the proximal axon, followed by a further gradual increase in the distal axon.
    Active cable modeling and experiments with partial channel block revealed that
    low axonal Na^+ conductance density was sufficient for reliability, but high Na^+
    density was necessary for both speed of propagation and fast-spiking AP phenotype.
    Our results suggest that a supercritical density of Na^+ channels compensates
    for the morphological properties of interneuron axons (small segmental diameter,
    extensive branching and high bouton density), ensuring fast AP propagation and
    high-frequency repetitive firing.
author:
- first_name: Hua
  full_name: Hu, Hua
  id: 4AC0145C-F248-11E8-B48F-1D18A9856A87
  last_name: Hu
- first_name: Peter M
  full_name: Jonas, Peter M
  id: 353C1B58-F248-11E8-B48F-1D18A9856A87
  last_name: Jonas
  orcid: 0000-0001-5001-4804
citation:
  ama: Hu H, Jonas PM. A supercritical density of Na^+ channels ensures fast signaling
    in GABAergic interneuron axons. <i>Nature Neuroscience</i>. 2014;17(5):686-693.
    doi:<a href="https://doi.org/10.1038/nn.3678">10.1038/nn.3678</a>
  apa: Hu, H., &#38; Jonas, P. M. (2014). A supercritical density of Na^+ channels
    ensures fast signaling in GABAergic interneuron axons. <i>Nature Neuroscience</i>.
    Nature Publishing Group. <a href="https://doi.org/10.1038/nn.3678">https://doi.org/10.1038/nn.3678</a>
  chicago: Hu, Hua, and Peter M Jonas. “A Supercritical Density of Na^+ Channels Ensures
    Fast Signaling in GABAergic Interneuron Axons.” <i>Nature Neuroscience</i>. Nature
    Publishing Group, 2014. <a href="https://doi.org/10.1038/nn.3678">https://doi.org/10.1038/nn.3678</a>.
  ieee: H. Hu and P. M. Jonas, “A supercritical density of Na^+ channels ensures fast
    signaling in GABAergic interneuron axons,” <i>Nature Neuroscience</i>, vol. 17,
    no. 5. Nature Publishing Group, pp. 686–693, 2014.
  ista: Hu H, Jonas PM. 2014. A supercritical density of Na^+ channels ensures fast
    signaling in GABAergic interneuron axons. Nature Neuroscience. 17(5), 686–693.
  mla: Hu, Hua, and Peter M. Jonas. “A Supercritical Density of Na^+ Channels Ensures
    Fast Signaling in GABAergic Interneuron Axons.” <i>Nature Neuroscience</i>, vol.
    17, no. 5, Nature Publishing Group, 2014, pp. 686–93, doi:<a href="https://doi.org/10.1038/nn.3678">10.1038/nn.3678</a>.
  short: H. Hu, P.M. Jonas, Nature Neuroscience 17 (2014) 686–693.
date_created: 2018-12-11T11:56:26Z
date_published: 2014-03-23T00:00:00Z
date_updated: 2021-01-12T06:56:08Z
day: '23'
department:
- _id: PeJo
doi: 10.1038/nn.3678
ec_funded: 1
intvolume: '        17'
issue: '5'
language:
- iso: eng
main_file_link:
- open_access: '1'
  url: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4286295/
month: '03'
oa: 1
oa_version: Submitted Version
page: 686-693
project:
- _id: 25C0F108-B435-11E9-9278-68D0E5697425
  call_identifier: FP7
  grant_number: '268548'
  name: Nanophysiology of fast-spiking, parvalbumin-expressing GABAergic interneurons
- _id: 25C26B1E-B435-11E9-9278-68D0E5697425
  call_identifier: FWF
  grant_number: P24909-B24
  name: Mechanisms of transmitter release at GABAergic synapses
publication: Nature Neuroscience
publication_identifier:
  issn:
  - '10976256'
publication_status: published
publisher: Nature Publishing Group
publist_id: '4733'
quality_controlled: '1'
scopus_import: 1
status: public
title: A supercritical density of Na^+ channels ensures fast signaling in GABAergic
  interneuron axons
type: journal_article
user_id: 4435EBFC-F248-11E8-B48F-1D18A9856A87
volume: 17
year: '2014'
...
---
_id: '2229'
abstract:
- lang: eng
  text: The distance between Ca^2+ channels and release sensors determines the speed
    and efficacy of synaptic transmission. Tight &quot;nanodomain&quot; channel-sensor
    coupling initiates transmitter release at synapses in the mature brain, whereas
    loose &quot;microdomain&quot; coupling appears restricted to early developmental
    stages. To probe the coupling configuration at a plastic synapse in the mature
    central nervous system, we performed paired recordings between mossy fiber terminals
    and CA3 pyramidal neurons in rat hippocampus. Millimolar concentrations of both
    the fast Ca^2+ chelator BAPTA [1,2-bis(2-aminophenoxy)ethane- N,N, N′,N′-tetraacetic
    acid] and the slow chelator EGTA efficiently suppressed transmitter release, indicating
    loose coupling between Ca^2+ channels and release sensors. Loose coupling enabled
    the control of initial release probability by fast endogenous Ca^2+ buffers and
    the generation of facilitation by buffer saturation. Thus, loose coupling provides
    the molecular framework for presynaptic plasticity.
author:
- first_name: Nicholas
  full_name: Vyleta, Nicholas
  id: 36C4978E-F248-11E8-B48F-1D18A9856A87
  last_name: Vyleta
- first_name: Peter M
  full_name: Jonas, Peter M
  id: 353C1B58-F248-11E8-B48F-1D18A9856A87
  last_name: Jonas
  orcid: 0000-0001-5001-4804
citation:
  ama: Vyleta N, Jonas PM. Loose coupling between Ca^2+ channels and release sensors
    at a plastic hippocampal synapse. <i>Science</i>. 2014;343(6171):665-670. doi:<a
    href="https://doi.org/10.1126/science.1244811">10.1126/science.1244811</a>
  apa: Vyleta, N., &#38; Jonas, P. M. (2014). Loose coupling between Ca^2+ channels
    and release sensors at a plastic hippocampal synapse. <i>Science</i>. American
    Association for the Advancement of Science. <a href="https://doi.org/10.1126/science.1244811">https://doi.org/10.1126/science.1244811</a>
  chicago: Vyleta, Nicholas, and Peter M Jonas. “Loose Coupling between Ca^2+ Channels
    and Release Sensors at a Plastic Hippocampal Synapse.” <i>Science</i>. American
    Association for the Advancement of Science, 2014. <a href="https://doi.org/10.1126/science.1244811">https://doi.org/10.1126/science.1244811</a>.
  ieee: N. Vyleta and P. M. Jonas, “Loose coupling between Ca^2+ channels and release
    sensors at a plastic hippocampal synapse,” <i>Science</i>, vol. 343, no. 6171.
    American Association for the Advancement of Science, pp. 665–670, 2014.
  ista: Vyleta N, Jonas PM. 2014. Loose coupling between Ca^2+ channels and release
    sensors at a plastic hippocampal synapse. Science. 343(6171), 665–670.
  mla: Vyleta, Nicholas, and Peter M. Jonas. “Loose Coupling between Ca^2+ Channels
    and Release Sensors at a Plastic Hippocampal Synapse.” <i>Science</i>, vol. 343,
    no. 6171, American Association for the Advancement of Science, 2014, pp. 665–70,
    doi:<a href="https://doi.org/10.1126/science.1244811">10.1126/science.1244811</a>.
  short: N. Vyleta, P.M. Jonas, Science 343 (2014) 665–670.
date_created: 2018-12-11T11:56:27Z
date_published: 2014-02-01T00:00:00Z
date_updated: 2021-01-12T06:56:09Z
day: '01'
department:
- _id: PeJo
doi: 10.1126/science.1244811
ec_funded: 1
intvolume: '       343'
issue: '6171'
language:
- iso: eng
main_file_link:
- open_access: '1'
  url: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3617475/
month: '02'
oa: 1
oa_version: Submitted Version
page: 665 - 670
project:
- _id: 25C26B1E-B435-11E9-9278-68D0E5697425
  call_identifier: FWF
  grant_number: P24909-B24
  name: Mechanisms of transmitter release at GABAergic synapses
- _id: 25C0F108-B435-11E9-9278-68D0E5697425
  call_identifier: FP7
  grant_number: '268548'
  name: Nanophysiology of fast-spiking, parvalbumin-expressing GABAergic interneurons
publication: Science
publication_identifier:
  issn:
  - '00368075'
publication_status: published
publisher: American Association for the Advancement of Science
publist_id: '4732'
quality_controlled: '1'
scopus_import: 1
status: public
title: Loose coupling between Ca^2+ channels and release sensors at a plastic hippocampal
  synapse
type: journal_article
user_id: 4435EBFC-F248-11E8-B48F-1D18A9856A87
volume: 343
year: '2014'
...
---
_id: '2230'
abstract:
- lang: eng
  text: Intracellular electrophysiological recordings provide crucial insights into
    elementary neuronal signals such as action potentials and synaptic currents. Analyzing
    and interpreting these signals is essential for a quantitative understanding of
    neuronal information processing, and requires both fast data visualization and
    ready access to complex analysis routines. To achieve this goal, we have developed
    Stimfit, a free software package for cellular neurophysiology with a Python scripting
    interface and a built-in Python shell. The program supports most standard file
    formats for cellular neurophysiology and other biomedical signals through the
    Biosig library. To quantify and interpret the activity of single neurons and communication
    between neurons, the program includes algorithms to characterize the kinetics
    of presynaptic action potentials and postsynaptic currents, estimate latencies
    between pre- and postsynaptic events, and detect spontaneously occurring events.
    We validate and benchmark these algorithms, give estimation errors, and provide
    sample use cases, showing that Stimfit represents an efficient, accessible and
    extensible way to accurately analyze and interpret neuronal signals.
article_number: '16'
author:
- first_name: José
  full_name: Guzmán, José
  id: 30CC5506-F248-11E8-B48F-1D18A9856A87
  last_name: Guzmán
- first_name: Alois
  full_name: Schlögl, Alois
  id: 45BF87EE-F248-11E8-B48F-1D18A9856A87
  last_name: Schlögl
  orcid: 0000-0002-5621-8100
- first_name: Christoph
  full_name: Schmidt Hieber, Christoph
  last_name: Schmidt Hieber
citation:
  ama: 'Guzmán J, Schlögl A, Schmidt Hieber C. Stimfit: Quantifying electrophysiological
    data with Python. <i>Frontiers in Neuroinformatics</i>. 2014;8(FEB). doi:<a href="https://doi.org/10.3389/fninf.2014.00016">10.3389/fninf.2014.00016</a>'
  apa: 'Guzmán, J., Schlögl, A., &#38; Schmidt Hieber, C. (2014). Stimfit: Quantifying
    electrophysiological data with Python. <i>Frontiers in Neuroinformatics</i>. Frontiers
    Research Foundation. <a href="https://doi.org/10.3389/fninf.2014.00016">https://doi.org/10.3389/fninf.2014.00016</a>'
  chicago: 'Guzmán, José, Alois Schlögl, and Christoph Schmidt Hieber. “Stimfit: Quantifying
    Electrophysiological Data with Python.” <i>Frontiers in Neuroinformatics</i>.
    Frontiers Research Foundation, 2014. <a href="https://doi.org/10.3389/fninf.2014.00016">https://doi.org/10.3389/fninf.2014.00016</a>.'
  ieee: 'J. Guzmán, A. Schlögl, and C. Schmidt Hieber, “Stimfit: Quantifying electrophysiological
    data with Python,” <i>Frontiers in Neuroinformatics</i>, vol. 8, no. FEB. Frontiers
    Research Foundation, 2014.'
  ista: 'Guzmán J, Schlögl A, Schmidt Hieber C. 2014. Stimfit: Quantifying electrophysiological
    data with Python. Frontiers in Neuroinformatics. 8(FEB), 16.'
  mla: 'Guzmán, José, et al. “Stimfit: Quantifying Electrophysiological Data with
    Python.” <i>Frontiers in Neuroinformatics</i>, vol. 8, no. FEB, 16, Frontiers
    Research Foundation, 2014, doi:<a href="https://doi.org/10.3389/fninf.2014.00016">10.3389/fninf.2014.00016</a>.'
  short: J. Guzmán, A. Schlögl, C. Schmidt Hieber, Frontiers in Neuroinformatics 8
    (2014).
date_created: 2018-12-11T11:56:27Z
date_published: 2014-02-21T00:00:00Z
date_updated: 2021-01-12T06:56:09Z
day: '21'
ddc:
- '570'
department:
- _id: ScienComp
- _id: PeJo
doi: 10.3389/fninf.2014.00016
file:
- access_level: open_access
  checksum: eeca00bba7232ff7d27db83321f6ea30
  content_type: application/pdf
  creator: system
  date_created: 2018-12-12T10:12:17Z
  date_updated: 2020-07-14T12:45:34Z
  file_id: '4935'
  file_name: IST-2016-425-v1+1_fninf-08-00016.pdf
  file_size: 2883372
  relation: main_file
file_date_updated: 2020-07-14T12:45:34Z
has_accepted_license: '1'
intvolume: '         8'
issue: FEB
language:
- iso: eng
month: '02'
oa: 1
oa_version: Published Version
publication: Frontiers in Neuroinformatics
publication_identifier:
  issn:
  - '16625196'
publication_status: published
publisher: Frontiers Research Foundation
publist_id: '4731'
pubrep_id: '425'
quality_controlled: '1'
scopus_import: 1
status: public
title: 'Stimfit: Quantifying electrophysiological data with Python'
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: '2014'
...
---
_id: '2254'
abstract:
- lang: eng
  text: Theta-gamma network oscillations are thought to represent key reference signals
    for information processing in neuronal ensembles, but the underlying synaptic
    mechanisms remain unclear. To address this question, we performed whole-cell (WC)
    patch-clamp recordings from mature hippocampal granule cells (GCs) in vivo in
    the dentate gyrus of anesthetized and awake rats. GCs in vivo fired action potentials
    at low frequency, consistent with sparse coding in the dentate gyrus. GCs were
    exposed to barrages of fast AMPAR-mediated excitatory postsynaptic currents (EPSCs),
    primarily relayed from the entorhinal cortex, and inhibitory postsynaptic currents
    (IPSCs), presumably generated by local interneurons. EPSCs exhibited coherence
    with the field potential predominantly in the theta frequency band, whereas IPSCs
    showed coherence primarily in the gamma range. Action potentials in GCs were phase
    locked to network oscillations. Thus, theta-gamma-modulated synaptic currents
    may provide a framework for sparse temporal coding of information in the dentate
    gyrus.
author:
- first_name: Alejandro
  full_name: Pernia-Andrade, Alejandro
  id: 36963E98-F248-11E8-B48F-1D18A9856A87
  last_name: Pernia-Andrade
- first_name: Peter M
  full_name: Jonas, Peter M
  id: 353C1B58-F248-11E8-B48F-1D18A9856A87
  last_name: Jonas
  orcid: 0000-0001-5001-4804
citation:
  ama: Pernia-Andrade A, Jonas PM. Theta-gamma-modulated synaptic currents in hippocampal
    granule cells in vivo define a mechanism for network oscillations. <i>Neuron</i>.
    2014;81(1):140-152. doi:<a href="https://doi.org/10.1016/j.neuron.2013.09.046">10.1016/j.neuron.2013.09.046</a>
  apa: Pernia-Andrade, A., &#38; Jonas, P. M. (2014). Theta-gamma-modulated synaptic
    currents in hippocampal granule cells in vivo define a mechanism for network oscillations.
    <i>Neuron</i>. Elsevier. <a href="https://doi.org/10.1016/j.neuron.2013.09.046">https://doi.org/10.1016/j.neuron.2013.09.046</a>
  chicago: Pernia-Andrade, Alejandro, and Peter M Jonas. “Theta-Gamma-Modulated Synaptic
    Currents in Hippocampal Granule Cells in Vivo Define a Mechanism for Network Oscillations.”
    <i>Neuron</i>. Elsevier, 2014. <a href="https://doi.org/10.1016/j.neuron.2013.09.046">https://doi.org/10.1016/j.neuron.2013.09.046</a>.
  ieee: A. Pernia-Andrade and P. M. Jonas, “Theta-gamma-modulated synaptic currents
    in hippocampal granule cells in vivo define a mechanism for network oscillations,”
    <i>Neuron</i>, vol. 81, no. 1. Elsevier, pp. 140–152, 2014.
  ista: Pernia-Andrade A, Jonas PM. 2014. Theta-gamma-modulated synaptic currents
    in hippocampal granule cells in vivo define a mechanism for network oscillations.
    Neuron. 81(1), 140–152.
  mla: Pernia-Andrade, Alejandro, and Peter M. Jonas. “Theta-Gamma-Modulated Synaptic
    Currents in Hippocampal Granule Cells in Vivo Define a Mechanism for Network Oscillations.”
    <i>Neuron</i>, vol. 81, no. 1, Elsevier, 2014, pp. 140–52, doi:<a href="https://doi.org/10.1016/j.neuron.2013.09.046">10.1016/j.neuron.2013.09.046</a>.
  short: A. Pernia-Andrade, P.M. Jonas, Neuron 81 (2014) 140–152.
date_created: 2018-12-11T11:56:35Z
date_published: 2014-01-08T00:00:00Z
date_updated: 2021-01-12T06:56:19Z
day: '08'
ddc:
- '570'
department:
- _id: PeJo
doi: 10.1016/j.neuron.2013.09.046
ec_funded: 1
file:
- access_level: open_access
  checksum: 438547cfcd9045a22f065f2019f07849
  content_type: application/pdf
  creator: system
  date_created: 2018-12-12T10:09:48Z
  date_updated: 2020-07-14T12:45:35Z
  file_id: '4773'
  file_name: IST-2016-422-v1+1_1-s2.0-S0896627313009227-main.pdf
  file_size: 4373072
  relation: main_file
file_date_updated: 2020-07-14T12:45:35Z
has_accepted_license: '1'
intvolume: '        81'
issue: '1'
language:
- iso: eng
month: '01'
oa: 1
oa_version: Published Version
page: 140 - 152
project:
- _id: 25C0F108-B435-11E9-9278-68D0E5697425
  call_identifier: FP7
  grant_number: '268548'
  name: Nanophysiology of fast-spiking, parvalbumin-expressing GABAergic interneurons
- _id: 25C26B1E-B435-11E9-9278-68D0E5697425
  call_identifier: FWF
  grant_number: P24909-B24
  name: Mechanisms of transmitter release at GABAergic synapses
publication: Neuron
publication_identifier:
  issn:
  - '08966273'
publication_status: published
publisher: Elsevier
publist_id: '4692'
pubrep_id: '422'
quality_controlled: '1'
scopus_import: 1
status: public
title: Theta-gamma-modulated synaptic currents in hippocampal granule cells in vivo
  define a mechanism for network oscillations
type: journal_article
user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87
volume: 81
year: '2014'
...
---
_id: '2285'
abstract:
- lang: eng
  text: GABAergic inhibitory interneurons control fundamental aspects of neuronal
    network function. Their functional roles are assumed to be defined by the identity
    of their input synapses, the architecture of their dendritic tree, the passive
    and active membrane properties and finally the nature of their postsynaptic targets.
    Indeed, interneurons display a high degree of morphological and physiological
    heterogeneity. However, whether their morphological and physiological characteristics
    are correlated and whether interneuron diversity can be described by a continuum
    of GABAergic cell types or by distinct classes has remained unclear. Here we perform
    a detailed morphological and physiological characterization of GABAergic cells
    in the dentate gyrus, the input region of the hippocampus. To achieve an unbiased
    and efficient sampling and classification we used knock-in mice expressing the
    enhanced green fluorescent protein (eGFP) in glutamate decarboxylase 67 (GAD67)-positive
    neurons and performed cluster analysis. We identified five interneuron classes,
    each of them characterized by a distinct set of anatomical and physiological parameters.
    Cross-correlation analysis further revealed a direct relation between morphological
    and physiological properties indicating that dentate gyrus interneurons fall into
    functionally distinct classes which may differentially control neuronal network
    activity.
acknowledgement: 'Funded by Deutsche Forschungsgemeinschaft. Grant Numbers: SFB 505,
  SFB 780, BA1582/2-1 Excellence Initiative of the German Research Foundation (Spemann
  Graduate School). Grant Number: GSC-4 Lichtenberg Professorship-Award (VW-Foundation);
  Schram-Foundation; Excellence Initiative Brain Links-Brain Tools. The authors thank
  Drs. Jonas-Frederic Sauer and Claudio Elgueta for critically reading the manuscript.
  They also thank Karin Winterhalter, Margit Northemann and Ulrich Nöller for technical
  assistance.'
author:
- first_name: Jonas
  full_name: Hosp, Jonas
  last_name: Hosp
- first_name: Michael
  full_name: Strüber, Michael
  last_name: Strüber
- first_name: Yuchio
  full_name: Yanagawa, Yuchio
  last_name: Yanagawa
- first_name: Kunihiko
  full_name: Obata, Kunihiko
  last_name: Obata
- first_name: Imre
  full_name: Vida, Imre
  last_name: Vida
- first_name: Peter M
  full_name: Jonas, Peter M
  id: 353C1B58-F248-11E8-B48F-1D18A9856A87
  last_name: Jonas
  orcid: 0000-0001-5001-4804
- first_name: Marlene
  full_name: Bartos, Marlene
  last_name: Bartos
citation:
  ama: Hosp J, Strüber M, Yanagawa Y, et al. Morpho-physiological criteria divide
    dentate gyrus interneurons into classes. <i>Hippocampus</i>. 2014;23(2):189-203.
    doi:<a href="https://doi.org/10.1002/hipo.22214">10.1002/hipo.22214</a>
  apa: Hosp, J., Strüber, M., Yanagawa, Y., Obata, K., Vida, I., Jonas, P. M., &#38;
    Bartos, M. (2014). Morpho-physiological criteria divide dentate gyrus interneurons
    into classes. <i>Hippocampus</i>. Wiley-Blackwell. <a href="https://doi.org/10.1002/hipo.22214">https://doi.org/10.1002/hipo.22214</a>
  chicago: Hosp, Jonas, Michael Strüber, Yuchio Yanagawa, Kunihiko Obata, Imre Vida,
    Peter M Jonas, and Marlene Bartos. “Morpho-Physiological Criteria Divide Dentate
    Gyrus Interneurons into Classes.” <i>Hippocampus</i>. Wiley-Blackwell, 2014. <a
    href="https://doi.org/10.1002/hipo.22214">https://doi.org/10.1002/hipo.22214</a>.
  ieee: J. Hosp <i>et al.</i>, “Morpho-physiological criteria divide dentate gyrus
    interneurons into classes,” <i>Hippocampus</i>, vol. 23, no. 2. Wiley-Blackwell,
    pp. 189–203, 2014.
  ista: Hosp J, Strüber M, Yanagawa Y, Obata K, Vida I, Jonas PM, Bartos M. 2014.
    Morpho-physiological criteria divide dentate gyrus interneurons into classes.
    Hippocampus. 23(2), 189–203.
  mla: Hosp, Jonas, et al. “Morpho-Physiological Criteria Divide Dentate Gyrus Interneurons
    into Classes.” <i>Hippocampus</i>, vol. 23, no. 2, Wiley-Blackwell, 2014, pp.
    189–203, doi:<a href="https://doi.org/10.1002/hipo.22214">10.1002/hipo.22214</a>.
  short: J. Hosp, M. Strüber, Y. Yanagawa, K. Obata, I. Vida, P.M. Jonas, M. Bartos,
    Hippocampus 23 (2014) 189–203.
date_created: 2018-12-11T11:56:46Z
date_published: 2014-02-01T00:00:00Z
date_updated: 2021-01-12T06:56:32Z
day: '01'
ddc:
- '570'
department:
- _id: PeJo
doi: 10.1002/hipo.22214
file:
- access_level: open_access
  checksum: ff6bc75a79dbc985a2e31b79253e6444
  content_type: application/pdf
  creator: system
  date_created: 2018-12-12T10:15:54Z
  date_updated: 2020-07-14T12:45:37Z
  file_id: '5178'
  file_name: IST-2016-461-v1+1_Hosp_et_al-2014-Hippocampus.pdf
  file_size: 801589
  relation: main_file
file_date_updated: 2020-07-14T12:45:37Z
has_accepted_license: '1'
intvolume: '        23'
issue: '2'
language:
- iso: eng
month: '02'
oa: 1
oa_version: Published Version
page: 189 - 203
publication: Hippocampus
publication_status: published
publisher: Wiley-Blackwell
publist_id: '4646'
pubrep_id: '461'
quality_controlled: '1'
scopus_import: 1
status: public
title: Morpho-physiological criteria divide dentate gyrus interneurons into classes
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: 3FFCCD3A-F248-11E8-B48F-1D18A9856A87
volume: 23
year: '2014'
...
---
_id: '10396'
abstract:
- lang: eng
  text: Stimfit is a free cross-platform software package for viewing and analyzing
    electrophysiological data. It supports most standard file types for cellular neurophysiology
    and other biomedical formats. Its analysis algorithms have been used and validated
    in several experimental laboratories. Its embedded Python scripting interface
    makes Stimfit highly extensible and customizable.
article_number: '000010151520134181'
article_processing_charge: No
article_type: original
author:
- first_name: Alois
  full_name: Schlögl, Alois
  id: 45BF87EE-F248-11E8-B48F-1D18A9856A87
  last_name: Schlögl
  orcid: 0000-0002-5621-8100
- first_name: Peter M
  full_name: Jonas, Peter M
  id: 353C1B58-F248-11E8-B48F-1D18A9856A87
  last_name: Jonas
  orcid: 0000-0001-5001-4804
- first_name: C.
  full_name: Schmidt-Hieber, C.
  last_name: Schmidt-Hieber
- first_name: S. J.
  full_name: Guzman, S. J.
  last_name: Guzman
citation:
  ama: 'Schlögl A, Jonas PM, Schmidt-Hieber C, Guzman SJ. Stimfit: A fast visualization
    and analysis environment for cellular neurophysiology. <i>Biomedical Engineering
    / Biomedizinische Technik</i>. 2013;58(SI-1-Track-G). doi:<a href="https://doi.org/10.1515/bmt-2013-4181">10.1515/bmt-2013-4181</a>'
  apa: 'Schlögl, A., Jonas, P. M., Schmidt-Hieber, C., &#38; Guzman, S. J. (2013).
    Stimfit: A fast visualization and analysis environment for cellular neurophysiology.
    <i>Biomedical Engineering / Biomedizinische Technik</i>. Graz, Austria: De Gruyter.
    <a href="https://doi.org/10.1515/bmt-2013-4181">https://doi.org/10.1515/bmt-2013-4181</a>'
  chicago: 'Schlögl, Alois, Peter M Jonas, C. Schmidt-Hieber, and S. J. Guzman. “Stimfit:
    A Fast Visualization and Analysis Environment for Cellular Neurophysiology.” <i>Biomedical
    Engineering / Biomedizinische Technik</i>. De Gruyter, 2013. <a href="https://doi.org/10.1515/bmt-2013-4181">https://doi.org/10.1515/bmt-2013-4181</a>.'
  ieee: 'A. Schlögl, P. M. Jonas, C. Schmidt-Hieber, and S. J. Guzman, “Stimfit: A
    fast visualization and analysis environment for cellular neurophysiology,” <i>Biomedical
    Engineering / Biomedizinische Technik</i>, vol. 58, no. SI-1-Track-G. De Gruyter,
    2013.'
  ista: 'Schlögl A, Jonas PM, Schmidt-Hieber C, Guzman SJ. 2013. Stimfit: A fast visualization
    and analysis environment for cellular neurophysiology. Biomedical Engineering
    / Biomedizinische Technik. 58(SI-1-Track-G), 000010151520134181.'
  mla: 'Schlögl, Alois, et al. “Stimfit: A Fast Visualization and Analysis Environment
    for Cellular Neurophysiology.” <i>Biomedical Engineering / Biomedizinische Technik</i>,
    vol. 58, no. SI-1-Track-G, 000010151520134181, De Gruyter, 2013, doi:<a href="https://doi.org/10.1515/bmt-2013-4181">10.1515/bmt-2013-4181</a>.'
  short: A. Schlögl, P.M. Jonas, C. Schmidt-Hieber, S.J. Guzman, Biomedical Engineering
    / Biomedizinische Technik 58 (2013).
conference:
  end_date: 2013-09-21
  location: Graz, Austria
  name: 'BMT: Biomedizinische Technik '
  start_date: 2013-09-19
date_created: 2021-12-01T14:35:35Z
date_published: 2013-08-01T00:00:00Z
date_updated: 2021-12-02T12:51:12Z
day: '01'
ddc:
- '005'
- '610'
department:
- _id: PeJo
doi: 10.1515/bmt-2013-4181
external_id:
  pmid:
  - '24042795'
file:
- access_level: open_access
  checksum: cdfc5339b530a25d6079f7223f0b1f16
  content_type: application/pdf
  creator: schloegl
  date_created: 2021-12-01T14:38:08Z
  date_updated: 2021-12-01T14:38:08Z
  file_id: '10397'
  file_name: Schloegl_Abstract-BMT2013.pdf
  file_size: 149825
  relation: main_file
  success: 1
file_date_updated: 2021-12-01T14:38:08Z
has_accepted_license: '1'
intvolume: '        58'
issue: SI-1-Track-G
keyword:
- biomedical engineering
- data analysis
- free software
language:
- iso: eng
month: '08'
oa: 1
oa_version: Submitted Version
pmid: 1
publication: Biomedical Engineering / Biomedizinische Technik
publication_identifier:
  eissn:
  - 1862-278X
  issn:
  - 0013-5585
publication_status: published
publisher: De Gruyter
quality_controlled: '1'
status: public
title: 'Stimfit: A fast visualization and analysis environment for cellular neurophysiology'
type: journal_article
user_id: 8b945eb4-e2f2-11eb-945a-df72226e66a9
volume: 58
year: '2013'
...
---
_id: '2954'
abstract:
- lang: eng
  text: Spontaneous postsynaptic currents (PSCs) provide key information about the
    mechanisms of synaptic transmission and the activity modes of neuronal networks.
    However, detecting spontaneous PSCs in vitro and in vivo has been challenging,
    because of the small amplitude, the variable kinetics, and the undefined time
    of generation of these events. Here, we describe a, to our knowledge, new method
    for detecting spontaneous synaptic events by deconvolution, using a template that
    approximates the average time course of spontaneous PSCs. A recorded PSC trace
    is deconvolved from the template, resulting in a series of delta-like functions.
    The maxima of these delta-like events are reliably detected, revealing the precise
    onset times of the spontaneous PSCs. Among all detection methods, the deconvolution-based
    method has a unique temporal resolution, allowing the detection of individual
    events in high-frequency bursts. Furthermore, the deconvolution-based method has
    a high amplitude resolution, because deconvolution can substantially increase
    the signal/noise ratio. When tested against previously published methods using
    experimental data, the deconvolution-based method was superior for spontaneous
    PSCs recorded in vivo. Using the high-resolution deconvolution-based detection
    algorithm, we show that the frequency of spontaneous excitatory postsynaptic currents
    in dentate gyrus granule cells is 4.5 times higher in vivo than in vitro.
acknowledgement: "This work was supported by the Deutsche Forschungsgemeinschaft (TR3/B10)
  and a European Research Council Advanced grant to P.J.\r\nWe thank H. Hu, S. J.
  Guzman, and C. Schmidt-Hieber for critically reading the manuscript, I. Koeva and
  F. Marr for technical support, and E. Kramberger for editorial assistance.\r\n"
author:
- first_name: Alejandro
  full_name: Pernia-Andrade, Alejandro
  id: 36963E98-F248-11E8-B48F-1D18A9856A87
  last_name: Pernia-Andrade
- first_name: Sarit
  full_name: Goswami, Sarit
  id: 3A578F32-F248-11E8-B48F-1D18A9856A87
  last_name: Goswami
- first_name: Yvonne
  full_name: Stickler, Yvonne
  id: 63B76600-E9CC-11E9-9B5F-82450873F7A1
  last_name: Stickler
- first_name: Ulrich
  full_name: Fröbe, Ulrich
  last_name: Fröbe
- first_name: Alois
  full_name: Schlögl, Alois
  id: 45BF87EE-F248-11E8-B48F-1D18A9856A87
  last_name: Schlögl
  orcid: 0000-0002-5621-8100
- first_name: Peter M
  full_name: Jonas, Peter M
  id: 353C1B58-F248-11E8-B48F-1D18A9856A87
  last_name: Jonas
  orcid: 0000-0001-5001-4804
citation:
  ama: Pernia-Andrade A, Goswami S, Stickler Y, Fröbe U, Schlögl A, Jonas PM. A deconvolution
    based method with high sensitivity and temporal resolution for detection of spontaneous
    synaptic currents in vitro and in vivo. <i>Biophysical Journal</i>. 2012;103(7):1429-1439.
    doi:<a href="https://doi.org/10.1016/j.bpj.2012.08.039">10.1016/j.bpj.2012.08.039</a>
  apa: Pernia-Andrade, A., Goswami, S., Stickler, Y., Fröbe, U., Schlögl, A., &#38;
    Jonas, P. M. (2012). A deconvolution based method with high sensitivity and temporal
    resolution for detection of spontaneous synaptic currents in vitro and in vivo.
    <i>Biophysical Journal</i>. Biophysical. <a href="https://doi.org/10.1016/j.bpj.2012.08.039">https://doi.org/10.1016/j.bpj.2012.08.039</a>
  chicago: Pernia-Andrade, Alejandro, Sarit Goswami, Yvonne Stickler, Ulrich Fröbe,
    Alois Schlögl, and Peter M Jonas. “A Deconvolution Based Method with High Sensitivity
    and Temporal Resolution for Detection of Spontaneous Synaptic Currents in Vitro
    and in Vivo.” <i>Biophysical Journal</i>. Biophysical, 2012. <a href="https://doi.org/10.1016/j.bpj.2012.08.039">https://doi.org/10.1016/j.bpj.2012.08.039</a>.
  ieee: A. Pernia-Andrade, S. Goswami, Y. Stickler, U. Fröbe, A. Schlögl, and P. M.
    Jonas, “A deconvolution based method with high sensitivity and temporal resolution
    for detection of spontaneous synaptic currents in vitro and in vivo,” <i>Biophysical
    Journal</i>, vol. 103, no. 7. Biophysical, pp. 1429–1439, 2012.
  ista: Pernia-Andrade A, Goswami S, Stickler Y, Fröbe U, Schlögl A, Jonas PM. 2012.
    A deconvolution based method with high sensitivity and temporal resolution for
    detection of spontaneous synaptic currents in vitro and in vivo. Biophysical Journal.
    103(7), 1429–1439.
  mla: Pernia-Andrade, Alejandro, et al. “A Deconvolution Based Method with High Sensitivity
    and Temporal Resolution for Detection of Spontaneous Synaptic Currents in Vitro
    and in Vivo.” <i>Biophysical Journal</i>, vol. 103, no. 7, Biophysical, 2012,
    pp. 1429–39, doi:<a href="https://doi.org/10.1016/j.bpj.2012.08.039">10.1016/j.bpj.2012.08.039</a>.
  short: A. Pernia-Andrade, S. Goswami, Y. Stickler, U. Fröbe, A. Schlögl, P.M. Jonas,
    Biophysical Journal 103 (2012) 1429–1439.
date_created: 2018-12-11T12:00:32Z
date_published: 2012-10-03T00:00:00Z
date_updated: 2021-01-12T07:40:01Z
day: '03'
department:
- _id: PeJo
- _id: ScienComp
doi: 10.1016/j.bpj.2012.08.039
external_id:
  pmid:
  - '23062335'
intvolume: '       103'
issue: '7'
language:
- iso: eng
main_file_link:
- open_access: '1'
  url: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3471482/
month: '10'
oa: 1
oa_version: Submitted Version
page: 1429 - 1439
pmid: 1
project:
- _id: 25BDE9A4-B435-11E9-9278-68D0E5697425
  grant_number: SFB-TR3-TP10B
  name: Glutamaterge synaptische Übertragung und Plastizität in hippocampalen Mikroschaltkreisen
publication: Biophysical Journal
publication_status: published
publisher: Biophysical
publist_id: '3774'
quality_controlled: '1'
scopus_import: 1
status: public
title: A deconvolution based method with high sensitivity and temporal resolution
  for detection of spontaneous synaptic currents in vitro and in vivo
type: journal_article
user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87
volume: 103
year: '2012'
...
---
_id: '2964'
abstract:
- lang: eng
  text: 'CA3 pyramidal neurons are important for memory formation and pattern completion
    in the hippocampal network. These neurons receive multiple excitatory inputs from
    numerous sources. Therefore, the rules of spatiotemporal integration of multiple
    synaptic inputs and propagation of action potentials are important to understand
    how CA3 neurons contribute to higher brain functions at cellular level. By using
    confocally targeted patch-clamp recording techniques, we investigated the biophysical
    properties of rat CA3 pyramidal neuron dendrites. We found two distinct dendritic
    domains critical for action potential initiation and propagation: In the proximal
    domain, action potentials initiated in the axon backpropagate actively with large
    amplitude and fast time course. In the distal domain, Na+-channel mediated dendritic
    spikes are efficiently evoked by local dendritic depolarization or waveforms mimicking
    synaptic events. These findings can be explained by a high Na+-to-K+ conductance
    density ratio of CA3 pyramidal neuron dendrites. The results challenge the prevailing
    view that proximal mossy fiber inputs activate CA3 pyramidal neurons more efficiently
    than distal perforant inputs by showing that the distal synapses trigger a different
    form of activity represented by dendritic spikes. The high probability of dendritic
    spike initiation in the distal area may enhance the computational power of CA3
    pyramidal neurons in the hippocampal network.  '
alternative_title:
- ISTA Thesis
article_processing_charge: No
author:
- first_name: Sooyun
  full_name: Kim, Sooyun
  id: 394AB1C8-F248-11E8-B48F-1D18A9856A87
  last_name: Kim
citation:
  ama: Kim S. Active properties of hippocampal CA3 pyramidal neuron dendrites. 2012.
  apa: Kim, S. (2012). <i>Active properties of hippocampal CA3 pyramidal neuron dendrites</i>.
    Institute of Science and Technology Austria.
  chicago: Kim, Sooyun. “Active Properties of Hippocampal CA3 Pyramidal Neuron Dendrites.”
    Institute of Science and Technology Austria, 2012.
  ieee: S. Kim, “Active properties of hippocampal CA3 pyramidal neuron dendrites,”
    Institute of Science and Technology Austria, 2012.
  ista: Kim S. 2012. Active properties of hippocampal CA3 pyramidal neuron dendrites.
    Institute of Science and Technology Austria.
  mla: Kim, Sooyun. <i>Active Properties of Hippocampal CA3 Pyramidal Neuron Dendrites</i>.
    Institute of Science and Technology Austria, 2012.
  short: S. Kim, Active Properties of Hippocampal CA3 Pyramidal Neuron Dendrites,
    Institute of Science and Technology Austria, 2012.
date_created: 2018-12-11T12:00:35Z
date_published: 2012-06-01T00:00:00Z
date_updated: 2023-09-07T11:43:51Z
day: '01'
degree_awarded: PhD
department:
- _id: PeJo
- _id: GradSch
language:
- iso: eng
month: '06'
oa_version: None
page: '65'
publication_identifier:
  issn:
  - 2663-337X
publication_status: published
publisher: Institute of Science and Technology Austria
publist_id: '3755'
related_material:
  record:
  - id: '3258'
    relation: part_of_dissertation
    status: public
status: public
supervisor:
- first_name: Peter M
  full_name: Jonas, Peter M
  id: 353C1B58-F248-11E8-B48F-1D18A9856A87
  last_name: Jonas
  orcid: 0000-0001-5001-4804
title: Active properties of hippocampal CA3 pyramidal neuron dendrites
type: dissertation
user_id: 8b945eb4-e2f2-11eb-945a-df72226e66a9
year: '2012'
...
---
_id: '2969'
abstract:
- lang: eng
  text: "The coupling between presynaptic Ca^(2+) channels and Ca^(2+) sensors of
    exocytosis is a key determinant of synaptic transmission. Evoked release from
    parvalbumin (PV)-expressing interneurons is triggered by nanodomain coupling of
    P/Q-type Ca^(2+) channels, whereas release from cholecystokinin (CCK)-containing
    interneurons is generated by microdomain coupling of N-type channels. Nanodomain
    coupling has several functional advantages, including speed and efficacy of transmission.
    One potential disadvantage is that stochastic\r\nopening of presynaptic Ca^(2+)
    channels may trigger spontaneous transmitter release. We addressed this possibility
    in rat hippocampal\r\ngranule cells, which receive converging inputs from different
    inhibitory sources. Both reduction of extracellular Ca^(2+) concentration and
    the unselective Ca^(2+) channel blocker Cd^(2+) reduced the frequency of miniature
    IPSCs (mIPSCs) in granule cells by ~50%, suggesting that the opening of presynaptic
    Ca^(2+) channels contributes to spontaneous release. Application of the selective
    P/Q-type Ca^(2+) channel blocker\r\nω-agatoxin IVa had no detectable effects,
    whereas both the N-type blocker ω-conotoxin GVIa and the L-type blocker nimodipine
    reduced\r\nmIPSC frequency. Furthermore, both the fast Ca^(2+) chelator BAPTA-AM
    and the slow chelator EGTA-AM reduced the mIPSC frequency,\r\nsuggesting that
    Ca^(2+)-dependent spontaneous release is triggered by microdomain rather than
    nanodomain coupling. The CB_(1) receptor\r\nagonist WIN 55212-2 also decreased
    spontaneous release; this effect was occluded by prior application of ω-conotoxin
    GVIa, suggesting that a major fraction of Ca^(2+)-dependent spontaneous release
    was generated at the terminals of CCK-expressing interneurons. Tonic inhibition
    generated by spontaneous opening of presynaptic N- and L-type Ca^(2+) channels
    may be important for hippocampal information processing.\r\n"
acknowledgement: This work was supported by grants from the Deutsche Forschungsgemeinschaft
  (TR 3/B10, Leibniz program, GSC-4 Spemann Graduate School) and the European Union
  (European Research Council Advanced Grant).
author:
- first_name: Sarit
  full_name: Goswami, Sarit
  id: 3A578F32-F248-11E8-B48F-1D18A9856A87
  last_name: Goswami
- first_name: Iancu
  full_name: Bucurenciu, Iancu
  last_name: Bucurenciu
- first_name: Peter M
  full_name: Jonas, Peter M
  id: 353C1B58-F248-11E8-B48F-1D18A9856A87
  last_name: Jonas
  orcid: 0000-0001-5001-4804
citation:
  ama: Goswami S, Bucurenciu I, Jonas PM. Miniature IPSCs in hippocampal granule cells
    are triggered by voltage-gated Ca^(2+) channels via microdomain coupling. <i>Journal
    of Neuroscience</i>. 2012;32(41):14294-14304. doi:<a href="https://doi.org/10.1523/JNEUROSCI.6104-11.2012">10.1523/JNEUROSCI.6104-11.2012</a>
  apa: Goswami, S., Bucurenciu, I., &#38; Jonas, P. M. (2012). Miniature IPSCs in
    hippocampal granule cells are triggered by voltage-gated Ca^(2+) channels via
    microdomain coupling. <i>Journal of Neuroscience</i>. Society for Neuroscience.
    <a href="https://doi.org/10.1523/JNEUROSCI.6104-11.2012">https://doi.org/10.1523/JNEUROSCI.6104-11.2012</a>
  chicago: Goswami, Sarit, Iancu Bucurenciu, and Peter M Jonas. “Miniature IPSCs in
    Hippocampal Granule Cells Are Triggered by Voltage-Gated Ca^(2+) Channels via
    Microdomain Coupling.” <i>Journal of Neuroscience</i>. Society for Neuroscience,
    2012. <a href="https://doi.org/10.1523/JNEUROSCI.6104-11.2012">https://doi.org/10.1523/JNEUROSCI.6104-11.2012</a>.
  ieee: S. Goswami, I. Bucurenciu, and P. M. Jonas, “Miniature IPSCs in hippocampal
    granule cells are triggered by voltage-gated Ca^(2+) channels via microdomain
    coupling,” <i>Journal of Neuroscience</i>, vol. 32, no. 41. Society for Neuroscience,
    pp. 14294–14304, 2012.
  ista: Goswami S, Bucurenciu I, Jonas PM. 2012. Miniature IPSCs in hippocampal granule
    cells are triggered by voltage-gated Ca^(2+) channels via microdomain coupling.
    Journal of Neuroscience. 32(41), 14294–14304.
  mla: Goswami, Sarit, et al. “Miniature IPSCs in Hippocampal Granule Cells Are Triggered
    by Voltage-Gated Ca^(2+) Channels via Microdomain Coupling.” <i>Journal of Neuroscience</i>,
    vol. 32, no. 41, Society for Neuroscience, 2012, pp. 14294–304, doi:<a href="https://doi.org/10.1523/JNEUROSCI.6104-11.2012">10.1523/JNEUROSCI.6104-11.2012</a>.
  short: S. Goswami, I. Bucurenciu, P.M. Jonas, Journal of Neuroscience 32 (2012)
    14294–14304.
date_created: 2018-12-11T12:00:36Z
date_published: 2012-10-10T00:00:00Z
date_updated: 2021-01-12T07:40:08Z
day: '10'
department:
- _id: PeJo
doi: 10.1523/JNEUROSCI.6104-11.2012
external_id:
  pmid:
  - '23055500'
intvolume: '        32'
issue: '41'
language:
- iso: eng
main_file_link:
- open_access: '1'
  url: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3632771/
month: '10'
oa: 1
oa_version: Submitted Version
page: 14294 - 14304
pmid: 1
project:
- _id: 25BDE9A4-B435-11E9-9278-68D0E5697425
  grant_number: SFB-TR3-TP10B
  name: Glutamaterge synaptische Übertragung und Plastizität in hippocampalen Mikroschaltkreisen
publication: Journal of Neuroscience
publication_status: published
publisher: Society for Neuroscience
publist_id: '3744'
quality_controlled: '1'
scopus_import: 1
status: public
title: Miniature IPSCs in hippocampal granule cells are triggered by voltage-gated
  Ca^(2+) channels via microdomain coupling
type: journal_article
user_id: 3E5EF7F0-F248-11E8-B48F-1D18A9856A87
volume: 32
year: '2012'
...
---
_id: '3121'
abstract:
- lang: eng
  text: Voltage-activated Ca(2+) channels (VACCs) mediate Ca(2+) influx to trigger
    action potential-evoked neurotransmitter release, but the mechanism by which Ca(2+)
    regulates spontaneous transmission is unclear. We found that VACCs are the major
    physiological triggers for spontaneous release at mouse neocortical inhibitory
    synapses. Moreover, despite the absence of a synchronizing action potential, we
    found that spontaneous fusion of a GABA-containing vesicle required the activation
    of multiple tightly coupled VACCs of variable type.
acknowledgement: "The work was supported by the US National Institutes of Health (DA027110
  and GM097433) and OCTRI. C.W. and N.P.V. were supported by a grant from the National
  Heart, Lung, and Blood Institute (T32HL033808).\r\nWe thank M. Andresen and K. Khodakhah
  for helpful comments. "
author:
- first_name: Courtney
  full_name: Williams, Courtney
  last_name: Williams
- first_name: Wenyan
  full_name: Chen, Wenyan
  last_name: Chen
- first_name: Chia
  full_name: Lee, Chia
  last_name: Lee
- first_name: Daniel
  full_name: Yaeger, Daniel
  last_name: Yaeger
- first_name: Nicholas
  full_name: Vyleta, Nicholas
  id: 36C4978E-F248-11E8-B48F-1D18A9856A87
  last_name: Vyleta
- first_name: Stephen
  full_name: Smith, Stephen
  last_name: Smith
citation:
  ama: Williams C, Chen W, Lee C, Yaeger D, Vyleta N, Smith S. Coactivation of multiple
    tightly coupled calcium channels triggers spontaneous release of GABA. <i>Nature
    Neuroscience</i>. 2012;15(9):1195-1197. doi:<a href="https://doi.org/10.1038/nn.3162">10.1038/nn.3162</a>
  apa: Williams, C., Chen, W., Lee, C., Yaeger, D., Vyleta, N., &#38; Smith, S. (2012).
    Coactivation of multiple tightly coupled calcium channels triggers spontaneous
    release of GABA. <i>Nature Neuroscience</i>. Nature Publishing Group. <a href="https://doi.org/10.1038/nn.3162">https://doi.org/10.1038/nn.3162</a>
  chicago: Williams, Courtney, Wenyan Chen, Chia Lee, Daniel Yaeger, Nicholas Vyleta,
    and Stephen Smith. “Coactivation of Multiple Tightly Coupled Calcium Channels
    Triggers Spontaneous Release of GABA.” <i>Nature Neuroscience</i>. Nature Publishing
    Group, 2012. <a href="https://doi.org/10.1038/nn.3162">https://doi.org/10.1038/nn.3162</a>.
  ieee: C. Williams, W. Chen, C. Lee, D. Yaeger, N. Vyleta, and S. Smith, “Coactivation
    of multiple tightly coupled calcium channels triggers spontaneous release of GABA,”
    <i>Nature Neuroscience</i>, vol. 15, no. 9. Nature Publishing Group, pp. 1195–1197,
    2012.
  ista: Williams C, Chen W, Lee C, Yaeger D, Vyleta N, Smith S. 2012. Coactivation
    of multiple tightly coupled calcium channels triggers spontaneous release of GABA.
    Nature Neuroscience. 15(9), 1195–1197.
  mla: Williams, Courtney, et al. “Coactivation of Multiple Tightly Coupled Calcium
    Channels Triggers Spontaneous Release of GABA.” <i>Nature Neuroscience</i>, vol.
    15, no. 9, Nature Publishing Group, 2012, pp. 1195–97, doi:<a href="https://doi.org/10.1038/nn.3162">10.1038/nn.3162</a>.
  short: C. Williams, W. Chen, C. Lee, D. Yaeger, N. Vyleta, S. Smith, Nature Neuroscience
    15 (2012) 1195–1197.
date_created: 2018-12-11T12:01:30Z
date_published: 2012-09-01T00:00:00Z
date_updated: 2021-01-12T07:41:12Z
day: '01'
department:
- _id: PeJo
doi: 10.1038/nn.3162
external_id:
  pmid:
  - '22842148'
intvolume: '        15'
issue: '9'
language:
- iso: eng
main_file_link:
- open_access: '1'
  url: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3431448/
month: '09'
oa: 1
oa_version: Submitted Version
page: 1195 - 1197
pmid: 1
publication: Nature Neuroscience
publication_status: published
publisher: Nature Publishing Group
publist_id: '3578'
quality_controlled: '1'
scopus_import: 1
status: public
title: Coactivation of multiple tightly coupled calcium channels triggers spontaneous
  release of GABA
type: journal_article
user_id: 3E5EF7F0-F248-11E8-B48F-1D18A9856A87
volume: 15
year: '2012'
...
---
_id: '3258'
abstract:
- lang: eng
  text: CA3 pyramidal neurons are important for memory formation and pattern completion
    in the hippocampal network. It is generally thought that proximal synapses from
    the mossy fibers activate these neurons most efficiently, whereas distal inputs
    from the perforant path have a weaker modulatory influence. We used confocally
    targeted patch-clamp recording from dendrites and axons to map the activation
    of rat CA3 pyramidal neurons at the subcellular level. Our results reveal two
    distinct dendritic domains. In the proximal domain, action potentials initiated
    in the axon backpropagate actively with large amplitude and fast time course.
    In the distal domain, Na+ channel–mediated dendritic spikes are efficiently initiated
    by waveforms mimicking synaptic events. CA3 pyramidal neuron dendrites showed
    a high Na+-to-K+ conductance density ratio, providing ideal conditions for active
    backpropagation and dendritic spike initiation. Dendritic spikes may enhance the
    computational power of CA3 pyramidal neurons in the hippocampal network.
acknowledgement: This work was supported by the Deutsche Forschungsgemeinschaft (TR
  3/B10) and the European Union (European Research Council Advanced grant to P.J.).
article_processing_charge: No
article_type: original
author:
- first_name: Sooyun
  full_name: Kim, Sooyun
  id: 394AB1C8-F248-11E8-B48F-1D18A9856A87
  last_name: Kim
- first_name: José
  full_name: Guzmán, José
  id: 30CC5506-F248-11E8-B48F-1D18A9856A87
  last_name: Guzmán
  orcid: 0000-0003-2209-5242
- first_name: Hua
  full_name: Hu, Hua
  id: 4AC0145C-F248-11E8-B48F-1D18A9856A87
  last_name: Hu
- first_name: Peter M
  full_name: Jonas, Peter M
  id: 353C1B58-F248-11E8-B48F-1D18A9856A87
  last_name: Jonas
  orcid: 0000-0001-5001-4804
citation:
  ama: Kim S, Guzmán J, Hu H, Jonas PM. Active dendrites support efficient initiation
    of dendritic spikes in hippocampal CA3 pyramidal neurons. <i>Nature Neuroscience</i>.
    2012;15(4):600-606. doi:<a href="https://doi.org/10.1038/nn.3060">10.1038/nn.3060</a>
  apa: Kim, S., Guzmán, J., Hu, H., &#38; Jonas, P. M. (2012). Active dendrites support
    efficient initiation of dendritic spikes in hippocampal CA3 pyramidal neurons.
    <i>Nature Neuroscience</i>. Nature Publishing Group. <a href="https://doi.org/10.1038/nn.3060">https://doi.org/10.1038/nn.3060</a>
  chicago: Kim, Sooyun, José Guzmán, Hua Hu, and Peter M Jonas. “Active Dendrites
    Support Efficient Initiation of Dendritic Spikes in Hippocampal CA3 Pyramidal
    Neurons.” <i>Nature Neuroscience</i>. Nature Publishing Group, 2012. <a href="https://doi.org/10.1038/nn.3060">https://doi.org/10.1038/nn.3060</a>.
  ieee: S. Kim, J. Guzmán, H. Hu, and P. M. Jonas, “Active dendrites support efficient
    initiation of dendritic spikes in hippocampal CA3 pyramidal neurons,” <i>Nature
    Neuroscience</i>, vol. 15, no. 4. Nature Publishing Group, pp. 600–606, 2012.
  ista: Kim S, Guzmán J, Hu H, Jonas PM. 2012. Active dendrites support efficient
    initiation of dendritic spikes in hippocampal CA3 pyramidal neurons. Nature Neuroscience.
    15(4), 600–606.
  mla: Kim, Sooyun, et al. “Active Dendrites Support Efficient Initiation of Dendritic
    Spikes in Hippocampal CA3 Pyramidal Neurons.” <i>Nature Neuroscience</i>, vol.
    15, no. 4, Nature Publishing Group, 2012, pp. 600–06, doi:<a href="https://doi.org/10.1038/nn.3060">10.1038/nn.3060</a>.
  short: S. Kim, J. Guzmán, H. Hu, P.M. Jonas, Nature Neuroscience 15 (2012) 600–606.
date_created: 2018-12-11T12:02:18Z
date_published: 2012-04-01T00:00:00Z
date_updated: 2023-09-07T11:43:52Z
day: '01'
department:
- _id: PeJo
doi: 10.1038/nn.3060
external_id:
  pmid:
  - '22388958'
intvolume: '        15'
issue: '4'
language:
- iso: eng
main_file_link:
- open_access: '1'
  url: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3617474/
month: '04'
oa: 1
oa_version: Published Version
page: 600 - 606
pmid: 1
project:
- _id: 25BDE9A4-B435-11E9-9278-68D0E5697425
  grant_number: SFB-TR3-TP10B
  name: Glutamaterge synaptische Übertragung und Plastizität in hippocampalen Mikroschaltkreisen
publication: Nature Neuroscience
publication_identifier:
  issn:
  - 1546-1726
publication_status: published
publisher: Nature Publishing Group
publist_id: '3390'
quality_controlled: '1'
related_material:
  record:
  - id: '2964'
    relation: dissertation_contains
    status: public
scopus_import: '1'
status: public
title: Active dendrites support efficient initiation of dendritic spikes in hippocampal
  CA3 pyramidal neurons
type: journal_article
user_id: 8b945eb4-e2f2-11eb-945a-df72226e66a9
volume: 15
year: '2012'
...
---
_id: '3317'
abstract:
- lang: eng
  text: The physical distance between presynaptic Ca2+ channels and the Ca2+ sensors
    that trigger exocytosis of neurotransmitter-containing vesicles is a key determinant
    of the signalling properties of synapses in the nervous system. Recent functional
    analysis indicates that in some fast central synapses, transmitter release is
    triggered by a small number of Ca2+ channels that are coupled to Ca2+ sensors
    at the nanometre scale. Molecular analysis suggests that this tight coupling is
    generated by protein–protein interactions involving Ca2+ channels, Ca2+ sensors
    and various other synaptic proteins. Nanodomain coupling has several functional
    advantages, as it increases the efficacy, speed and energy efficiency of synaptic
    transmission.
acknowledgement: "Work of the authors was funded by grants of the Deutsche Forschungsgemeinschaft
  to P.J. (grants SFB 780/A5, TR 3/B10 and the Leibniz programme), a European Research
  Council Advanced grant to P.J. and a Swiss National Foundation fellowship to E.E.\r\nWe
  thank D. Tsien and E. Neher for their comments on this Review, J. Guzmán and A.
  Pernía-Andrade for reading earlier versions and E. Kramberger for perfect editorial
  support. We apologize that owing to space constraints, not all relevant papers could
  be cited.\r\n"
author:
- first_name: Emmanuel
  full_name: Eggermann, Emmanuel
  id: 34DACA34-E9AE-11E9-849C-D35BD8ADC20C
  last_name: Eggermann
- first_name: Iancu
  full_name: Bucurenciu, Iancu
  id: 4BD1D872-E9AE-11E9-9EE9-8BF4597A9E2A
  last_name: Bucurenciu
- first_name: Sarit
  full_name: Goswami, Sarit
  id: 3A578F32-F248-11E8-B48F-1D18A9856A87
  last_name: Goswami
- first_name: Peter M
  full_name: Jonas, Peter M
  id: 353C1B58-F248-11E8-B48F-1D18A9856A87
  last_name: Jonas
  orcid: 0000-0001-5001-4804
citation:
  ama: Eggermann E, Bucurenciu I, Goswami S, Jonas PM. Nanodomain coupling between
    Ca(2+) channels and sensors of exocytosis at fast mammalian synapses. <i>Nature
    Reviews Neuroscience</i>. 2012;13(1):7-21. doi:<a href="https://doi.org/10.1038/nrn3125">10.1038/nrn3125</a>
  apa: Eggermann, E., Bucurenciu, I., Goswami, S., &#38; Jonas, P. M. (2012). Nanodomain
    coupling between Ca(2+) channels and sensors of exocytosis at fast mammalian synapses.
    <i>Nature Reviews Neuroscience</i>. Nature Publishing Group. <a href="https://doi.org/10.1038/nrn3125">https://doi.org/10.1038/nrn3125</a>
  chicago: Eggermann, Emmanuel, Iancu Bucurenciu, Sarit Goswami, and Peter M Jonas.
    “Nanodomain Coupling between Ca(2+) Channels and Sensors of Exocytosis at Fast
    Mammalian Synapses.” <i>Nature Reviews Neuroscience</i>. Nature Publishing Group,
    2012. <a href="https://doi.org/10.1038/nrn3125">https://doi.org/10.1038/nrn3125</a>.
  ieee: E. Eggermann, I. Bucurenciu, S. Goswami, and P. M. Jonas, “Nanodomain coupling
    between Ca(2+) channels and sensors of exocytosis at fast mammalian synapses,”
    <i>Nature Reviews Neuroscience</i>, vol. 13, no. 1. Nature Publishing Group, pp.
    7–21, 2012.
  ista: Eggermann E, Bucurenciu I, Goswami S, Jonas PM. 2012. Nanodomain coupling
    between Ca(2+) channels and sensors of exocytosis at fast mammalian synapses.
    Nature Reviews Neuroscience. 13(1), 7–21.
  mla: Eggermann, Emmanuel, et al. “Nanodomain Coupling between Ca(2+) Channels and
    Sensors of Exocytosis at Fast Mammalian Synapses.” <i>Nature Reviews Neuroscience</i>,
    vol. 13, no. 1, Nature Publishing Group, 2012, pp. 7–21, doi:<a href="https://doi.org/10.1038/nrn3125">10.1038/nrn3125</a>.
  short: E. Eggermann, I. Bucurenciu, S. Goswami, P.M. Jonas, Nature Reviews Neuroscience
    13 (2012) 7–21.
date_created: 2018-12-11T12:02:38Z
date_published: 2012-01-01T00:00:00Z
date_updated: 2021-01-12T07:42:36Z
day: '01'
ddc:
- '570'
department:
- _id: PeJo
doi: 10.1038/nrn3125
file:
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has_accepted_license: '1'
intvolume: '        13'
issue: '1'
language:
- iso: eng
month: '01'
oa: 1
oa_version: Submitted Version
page: 7 - 21
project:
- _id: 25BC64A8-B435-11E9-9278-68D0E5697425
  grant_number: JO_780/A5
  name: Synaptic Mechanisms of Neuronal Network Function
- _id: 25BDE9A4-B435-11E9-9278-68D0E5697425
  grant_number: SFB-TR3-TP10B
  name: Glutamaterge synaptische Übertragung und Plastizität in hippocampalen Mikroschaltkreisen
publication: Nature Reviews Neuroscience
publication_status: published
publisher: Nature Publishing Group
publist_id: '3322'
pubrep_id: '820'
quality_controlled: '1'
scopus_import: 1
status: public
title: Nanodomain coupling between Ca(2+) channels and sensors of exocytosis at fast
  mammalian synapses
type: journal_article
user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87
volume: 13
year: '2012'
...
---
_id: '493'
abstract:
- lang: eng
  text: 'The BCI competition IV stands in the tradition of prior BCI competitions
    that aim to provide high quality neuroscientific data for open access to the scientific
    community. As experienced already in prior competitions not only scientists from
    the narrow field of BCI compete, but scholars with a broad variety of backgrounds
    and nationalities. They include high specialists as well as students.The goals
    of all BCI competitions have always been to challenge with respect to novel paradigms
    and complex data. We report on the following challenges: (1) asynchronous data,
    (2) synthetic, (3) multi-class continuous data, (4) sessionto-session transfer,
    (5) directionally modulated MEG, (6) finger movements recorded by ECoG. As after
    past competitions, our hope is that winning entries may enhance the analysis methods
    of future BCIs.'
acknowledgement: "The studies were in part or completely supported by the Bundesministerium
  für Bildung und Forschung (BMBF), Fkz 01IB001A, 01GQ0850, by the German Science
  Foundation (DFG, contract MU 987/3-2), by the European ICT Programme Projects FP7-224631
  and 216886, the World Class University Program through the National Research Foundation
  of Korea funded by the Ministry of Education, Science, and Technology (Grant R31-10008),
  the US Army Research Office [W911NF-08-1-0216 (Gerwin Schalk) and W911NF-07-1-0415
  (Gerwin Schalk)] and the NIH [EB006356 (Gerwin Schalk) and EB000856 (Gerwin Schalk),
  the WIN-Kolleg of the Heidelberg Academy of Sciences and Humanities, German Federal
  Ministry of Education and Research grants 01GQ0420, 01GQ0761, 01GQ0762, and 01GQ0830,
  German Research Foundation grants 550/B5 and C6, and by a scholarship from the German
  National Academic Foundation. This paper only reflects the authors’ views and funding
  agencies are not liable for any use that may be made of the information contained
  herein.\r\n"
article_number: '55'
author:
- first_name: Michael
  full_name: Tangermann, Michael
  last_name: Tangermann
- first_name: Klaus
  full_name: Müller, Klaus
  last_name: Müller
- first_name: Ad
  full_name: Aertsen, Ad
  last_name: Aertsen
- first_name: Niels
  full_name: Birbaumer, Niels
  last_name: Birbaumer
- first_name: Christoph
  full_name: Braun, Christoph
  last_name: Braun
- first_name: Clemens
  full_name: Brunner, Clemens
  last_name: Brunner
- first_name: Robert
  full_name: Leeb, Robert
  last_name: Leeb
- first_name: Carsten
  full_name: Mehring, Carsten
  last_name: Mehring
- first_name: Kai
  full_name: Miller, Kai
  last_name: Miller
- first_name: Gernot
  full_name: Müller Putz, Gernot
  last_name: Müller Putz
- first_name: Guido
  full_name: Nolte, Guido
  last_name: Nolte
- first_name: Gert
  full_name: Pfurtscheller, Gert
  last_name: Pfurtscheller
- first_name: Hubert
  full_name: Preissl, Hubert
  last_name: Preissl
- first_name: Gerwin
  full_name: Schalk, Gerwin
  last_name: Schalk
- first_name: Alois
  full_name: Schlögl, Alois
  id: 45BF87EE-F248-11E8-B48F-1D18A9856A87
  last_name: Schlögl
  orcid: 0000-0002-5621-8100
- first_name: Carmen
  full_name: Vidaurre, Carmen
  last_name: Vidaurre
- first_name: Stephan
  full_name: Waldert, Stephan
  last_name: Waldert
- first_name: Benjamin
  full_name: Blankertz, Benjamin
  last_name: Blankertz
citation:
  ama: Tangermann M, Müller K, Aertsen A, et al. Review of the BCI competition IV.
    <i>Frontiers in Neuroscience</i>. 2012;6. doi:<a href="https://doi.org/10.3389/fnins.2012.00055">10.3389/fnins.2012.00055</a>
  apa: Tangermann, M., Müller, K., Aertsen, A., Birbaumer, N., Braun, C., Brunner,
    C., … Blankertz, B. (2012). Review of the BCI competition IV. <i>Frontiers in
    Neuroscience</i>. Frontiers Research Foundation. <a href="https://doi.org/10.3389/fnins.2012.00055">https://doi.org/10.3389/fnins.2012.00055</a>
  chicago: Tangermann, Michael, Klaus Müller, Ad Aertsen, Niels Birbaumer, Christoph
    Braun, Clemens Brunner, Robert Leeb, et al. “Review of the BCI Competition IV.”
    <i>Frontiers in Neuroscience</i>. Frontiers Research Foundation, 2012. <a href="https://doi.org/10.3389/fnins.2012.00055">https://doi.org/10.3389/fnins.2012.00055</a>.
  ieee: M. Tangermann <i>et al.</i>, “Review of the BCI competition IV,” <i>Frontiers
    in Neuroscience</i>, vol. 6. Frontiers Research Foundation, 2012.
  ista: Tangermann M, Müller K, Aertsen A, Birbaumer N, Braun C, Brunner C, Leeb R,
    Mehring C, Miller K, Müller Putz G, Nolte G, Pfurtscheller G, Preissl H, Schalk
    G, Schlögl A, Vidaurre C, Waldert S, Blankertz B. 2012. Review of the BCI competition
    IV. Frontiers in Neuroscience. 6, 55.
  mla: Tangermann, Michael, et al. “Review of the BCI Competition IV.” <i>Frontiers
    in Neuroscience</i>, vol. 6, 55, Frontiers Research Foundation, 2012, doi:<a href="https://doi.org/10.3389/fnins.2012.00055">10.3389/fnins.2012.00055</a>.
  short: M. Tangermann, K. Müller, A. Aertsen, N. Birbaumer, C. Braun, C. Brunner,
    R. Leeb, C. Mehring, K. Miller, G. Müller Putz, G. Nolte, G. Pfurtscheller, H.
    Preissl, G. Schalk, A. Schlögl, C. Vidaurre, S. Waldert, B. Blankertz, Frontiers
    in Neuroscience 6 (2012).
date_created: 2018-12-11T11:46:46Z
date_published: 2012-07-13T00:00:00Z
date_updated: 2021-01-12T08:01:03Z
day: '13'
ddc:
- '004'
department:
- _id: ScienComp
- _id: PeJo
doi: 10.3389/fnins.2012.00055
file:
- access_level: open_access
  checksum: 195238221c4b0b0f4035f6f6c16ea17c
  content_type: application/pdf
  creator: system
  date_created: 2018-12-12T10:18:34Z
  date_updated: 2020-07-14T12:46:35Z
  file_id: '5356'
  file_name: IST-2018-945-v1+1_2012_Schloegl_Review_of.pdf
  file_size: 2693701
  relation: main_file
file_date_updated: 2020-07-14T12:46:35Z
has_accepted_license: '1'
intvolume: '         6'
language:
- iso: eng
month: '07'
oa: 1
oa_version: Published Version
publication: Frontiers in Neuroscience
publication_status: published
publisher: Frontiers Research Foundation
publist_id: '7327'
pubrep_id: '945'
quality_controlled: '1'
scopus_import: 1
status: public
title: Review of the BCI competition IV
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: 3E5EF7F0-F248-11E8-B48F-1D18A9856A87
volume: 6
year: '2012'
...
---
_id: '3318'
abstract:
- lang: eng
  text: Parvalbumin is thought to act in a manner similar to EGTA, but how a slow
    Ca2+ buffer affects nanodomain-coupling regimes at GABAergic synapses is unclear.
    Direct measurements of parvalbumin concentration and paired recordings in rodent
    hippocampus and cerebellum revealed that parvalbumin affects synaptic dynamics
    only when expressed at high levels. Modeling suggests that, in high concentrations,
    parvalbumin may exert BAPTA-like effects, modulating nanodomain coupling via competition
    with local saturation of endogenous fixed buffers.
author:
- first_name: Emmanuel
  full_name: Eggermann, Emmanuel
  last_name: Eggermann
- first_name: Peter M
  full_name: Jonas, Peter M
  id: 353C1B58-F248-11E8-B48F-1D18A9856A87
  last_name: Jonas
  orcid: 0000-0001-5001-4804
citation:
  ama: Eggermann E, Jonas PM. How the “slow” Ca(2+) buffer parvalbumin affects transmitter
    release in nanodomain coupling regimes at GABAergic synapses. <i>Nature Neuroscience</i>.
    2011;15:20-22. doi:<a href="https://doi.org/10.1038/nn.3002">10.1038/nn.3002</a>
  apa: Eggermann, E., &#38; Jonas, P. M. (2011). How the “slow” Ca(2+) buffer parvalbumin
    affects transmitter release in nanodomain coupling regimes at GABAergic synapses.
    <i>Nature Neuroscience</i>. Nature Publishing Group. <a href="https://doi.org/10.1038/nn.3002">https://doi.org/10.1038/nn.3002</a>
  chicago: Eggermann, Emmanuel, and Peter M Jonas. “How the ‘Slow’ Ca(2+) Buffer Parvalbumin
    Affects Transmitter Release in Nanodomain Coupling Regimes at GABAergic Synapses.”
    <i>Nature Neuroscience</i>. Nature Publishing Group, 2011. <a href="https://doi.org/10.1038/nn.3002">https://doi.org/10.1038/nn.3002</a>.
  ieee: E. Eggermann and P. M. Jonas, “How the ‘slow’ Ca(2+) buffer parvalbumin affects
    transmitter release in nanodomain coupling regimes at GABAergic synapses,” <i>Nature
    Neuroscience</i>, vol. 15. Nature Publishing Group, pp. 20–22, 2011.
  ista: Eggermann E, Jonas PM. 2011. How the “slow” Ca(2+) buffer parvalbumin affects
    transmitter release in nanodomain coupling regimes at GABAergic synapses. Nature
    Neuroscience. 15, 20–22.
  mla: Eggermann, Emmanuel, and Peter M. Jonas. “How the ‘Slow’ Ca(2+) Buffer Parvalbumin
    Affects Transmitter Release in Nanodomain Coupling Regimes at GABAergic Synapses.”
    <i>Nature Neuroscience</i>, vol. 15, Nature Publishing Group, 2011, pp. 20–22,
    doi:<a href="https://doi.org/10.1038/nn.3002">10.1038/nn.3002</a>.
  short: E. Eggermann, P.M. Jonas, Nature Neuroscience 15 (2011) 20–22.
date_created: 2018-12-11T12:02:38Z
date_published: 2011-12-04T00:00:00Z
date_updated: 2021-01-12T07:42:37Z
day: '04'
department:
- _id: PeJo
doi: 10.1038/nn.3002
intvolume: '        15'
language:
- iso: eng
main_file_link:
- open_access: '1'
  url: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3631701/
month: '12'
oa: 1
oa_version: Submitted Version
page: 20 - 22
publication: Nature Neuroscience
publication_status: published
publisher: Nature Publishing Group
publist_id: '3321'
quality_controlled: '1'
scopus_import: 1
status: public
title: How the “slow” Ca(2+) buffer parvalbumin affects transmitter release in nanodomain
  coupling regimes at GABAergic synapses
type: journal_article
user_id: 4435EBFC-F248-11E8-B48F-1D18A9856A87
volume: 15
year: '2011'
...
---
_id: '469'
abstract:
- lang: eng
  text: 'Spontaneous release of glutamate is important for maintaining synaptic strength
    and controlling spike timing in the brain. Mechanisms regulating spontaneous exocytosis
    remain poorly understood. Extracellular calcium concentration ([Ca2+]o) regulates
    Ca2+ entry through voltage-activated calcium channels (VACCs) and consequently
    is a pivotal determinant of action potential-evoked vesicle fusion. Extracellular
    Ca 2+ also enhances spontaneous release, but via unknown mechanisms. Here we report
    that external Ca2+ triggers spontaneous glutamate release more weakly than evoked
    release in mouse neocortical neurons. Blockade of VACCs has no effect on the spontaneous
    release rate or its dependence on [Ca2+]o. Intracellular [Ca2+] slowly increases
    in a minority of neurons following increases in [Ca2+]o. Furthermore, the enhancement
    of spontaneous release by extracellular calcium is insensitive to chelation of
    intracellular calcium by BAPTA. Activation of the calcium-sensing receptor (CaSR),
    a G-protein-coupled receptor present in nerve terminals, by several specific agonists
    increased spontaneous glutamate release. The frequency of spontaneous synaptic
    transmission was decreased in CaSR mutant neurons. The concentration-effect relationship
    for extracellular calcium regulation of spontaneous release was well described
    by a combination of CaSR-dependent and CaSR-independent mechanisms. Overall these
    results indicate that extracellular Ca2+ does not trigger spontaneous glutamate
    release by simply increasing calcium influx but stimulates CaSR and thereby promotes
    resting spontaneous glutamate release. '
author:
- first_name: Nicholas
  full_name: Vyleta, Nicholas
  id: 36C4978E-F248-11E8-B48F-1D18A9856A87
  last_name: Vyleta
- first_name: Stephen
  full_name: Smith, Stephen
  last_name: Smith
citation:
  ama: Vyleta N, Smith S. Spontaneous glutamate release is independent of calcium
    influx and tonically activated by the calcium-sensing receptor. <i>European Journal
    of Neuroscience</i>. 2011;31(12):4593-4606. doi:<a href="https://doi.org/10.1523/JNEUROSCI.6398-10.2011">10.1523/JNEUROSCI.6398-10.2011</a>
  apa: Vyleta, N., &#38; Smith, S. (2011). Spontaneous glutamate release is independent
    of calcium influx and tonically activated by the calcium-sensing receptor. <i>European
    Journal of Neuroscience</i>. Wiley-Blackwell. <a href="https://doi.org/10.1523/JNEUROSCI.6398-10.2011">https://doi.org/10.1523/JNEUROSCI.6398-10.2011</a>
  chicago: Vyleta, Nicholas, and Stephen Smith. “Spontaneous Glutamate Release Is
    Independent of Calcium Influx and Tonically Activated by the Calcium-Sensing Receptor.”
    <i>European Journal of Neuroscience</i>. Wiley-Blackwell, 2011. <a href="https://doi.org/10.1523/JNEUROSCI.6398-10.2011">https://doi.org/10.1523/JNEUROSCI.6398-10.2011</a>.
  ieee: N. Vyleta and S. Smith, “Spontaneous glutamate release is independent of calcium
    influx and tonically activated by the calcium-sensing receptor,” <i>European Journal
    of Neuroscience</i>, vol. 31, no. 12. Wiley-Blackwell, pp. 4593–4606, 2011.
  ista: Vyleta N, Smith S. 2011. Spontaneous glutamate release is independent of calcium
    influx and tonically activated by the calcium-sensing receptor. European Journal
    of Neuroscience. 31(12), 4593–4606.
  mla: Vyleta, Nicholas, and Stephen Smith. “Spontaneous Glutamate Release Is Independent
    of Calcium Influx and Tonically Activated by the Calcium-Sensing Receptor.” <i>European
    Journal of Neuroscience</i>, vol. 31, no. 12, Wiley-Blackwell, 2011, pp. 4593–606,
    doi:<a href="https://doi.org/10.1523/JNEUROSCI.6398-10.2011">10.1523/JNEUROSCI.6398-10.2011</a>.
  short: N. Vyleta, S. Smith, European Journal of Neuroscience 31 (2011) 4593–4606.
date_created: 2018-12-11T11:46:39Z
date_published: 2011-03-23T00:00:00Z
date_updated: 2021-01-12T08:00:49Z
day: '23'
department:
- _id: PeJo
doi: 10.1523/JNEUROSCI.6398-10.2011
intvolume: '        31'
issue: '12'
language:
- iso: eng
main_file_link:
- open_access: '1'
  url: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3097128/
month: '03'
oa: 1
oa_version: Submitted Version
page: 4593 - 4606
publication: European Journal of Neuroscience
publication_status: published
publisher: Wiley-Blackwell
publist_id: '7353'
quality_controlled: '1'
scopus_import: 1
status: public
title: Spontaneous glutamate release is independent of calcium influx and tonically
  activated by the calcium-sensing receptor
type: journal_article
user_id: 4435EBFC-F248-11E8-B48F-1D18A9856A87
volume: 31
year: '2011'
...
---
_id: '490'
abstract:
- lang: eng
  text: 'BioSig is an open source software library for biomedical signal processing.
    The aim of the BioSig project is to foster research in biomedical signal processing
    by providing free and open source software tools for many different application
    areas. Some of the areas where BioSig can be employed are neuroinformatics, brain-computer
    interfaces, neurophysiology, psychology, cardiovascular systems, and sleep research.
    Moreover, the analysis of biosignals such as the electroencephalogram (EEG), electrocorticogram
    (ECoG), electrocardiogram (ECG), electrooculogram (EOG), electromyogram (EMG),
    or respiration signals is a very relevant element of the BioSig project. Specifically,
    BioSig provides solutions for data acquisition, artifact processing, quality control,
    feature extraction, classification, modeling, and data visualization, to name
    a few. In this paper, we highlight several methods to help students and researchers
    to work more efficiently with biomedical signals. '
article_number: '935364'
author:
- first_name: Alois
  full_name: Schlögl, Alois
  id: 45BF87EE-F248-11E8-B48F-1D18A9856A87
  last_name: Schlögl
  orcid: 0000-0002-5621-8100
- first_name: Carmen
  full_name: Vidaurre, Carmen
  last_name: Vidaurre
- first_name: Tilmann
  full_name: Sander, Tilmann
  last_name: Sander
citation:
  ama: 'Schlögl A, Vidaurre C, Sander T. BioSig: The free and open source software
    library for biomedical signal processing. <i>Computational Intelligence and Neuroscience</i>.
    2011;2011. doi:<a href="https://doi.org/10.1155/2011/935364">10.1155/2011/935364</a>'
  apa: 'Schlögl, A., Vidaurre, C., &#38; Sander, T. (2011). BioSig: The free and open
    source software library for biomedical signal processing. <i>Computational Intelligence
    and Neuroscience</i>. Hindawi Publishing Corporation. <a href="https://doi.org/10.1155/2011/935364">https://doi.org/10.1155/2011/935364</a>'
  chicago: 'Schlögl, Alois, Carmen Vidaurre, and Tilmann Sander. “BioSig: The Free
    and Open Source Software Library for Biomedical Signal Processing.” <i>Computational
    Intelligence and Neuroscience</i>. Hindawi Publishing Corporation, 2011. <a href="https://doi.org/10.1155/2011/935364">https://doi.org/10.1155/2011/935364</a>.'
  ieee: 'A. Schlögl, C. Vidaurre, and T. Sander, “BioSig: The free and open source
    software library for biomedical signal processing,” <i>Computational Intelligence
    and Neuroscience</i>, vol. 2011. Hindawi Publishing Corporation, 2011.'
  ista: 'Schlögl A, Vidaurre C, Sander T. 2011. BioSig: The free and open source software
    library for biomedical signal processing. Computational Intelligence and Neuroscience.
    2011, 935364.'
  mla: 'Schlögl, Alois, et al. “BioSig: The Free and Open Source Software Library
    for Biomedical Signal Processing.” <i>Computational Intelligence and Neuroscience</i>,
    vol. 2011, 935364, Hindawi Publishing Corporation, 2011, doi:<a href="https://doi.org/10.1155/2011/935364">10.1155/2011/935364</a>.'
  short: A. Schlögl, C. Vidaurre, T. Sander, Computational Intelligence and Neuroscience
    2011 (2011).
date_created: 2018-12-11T11:46:45Z
date_published: 2011-01-01T00:00:00Z
date_updated: 2021-01-12T08:01:02Z
day: '01'
ddc:
- '005'
department:
- _id: ScienComp
- _id: PeJo
doi: 10.1155/2011/935364
file:
- access_level: open_access
  checksum: 8263bbf255171f2054f43f3db5f53b6e
  content_type: application/pdf
  creator: system
  date_created: 2018-12-12T10:07:44Z
  date_updated: 2020-07-14T12:46:35Z
  file_id: '4642'
  file_name: IST-2018-947-v1+1_2011_Schloegl_BioSig.pdf
  file_size: 2863551
  relation: main_file
file_date_updated: 2020-07-14T12:46:35Z
has_accepted_license: '1'
intvolume: '      2011'
language:
- iso: eng
month: '01'
oa: 1
oa_version: Published Version
publication: Computational Intelligence and Neuroscience
publication_status: published
publisher: Hindawi Publishing Corporation
publist_id: '7330'
pubrep_id: '947'
quality_controlled: '1'
scopus_import: 1
status: public
title: 'BioSig: The free and open source software library for biomedical signal processing'
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: 2011
year: '2011'
...
---
_id: '3369'
abstract:
- lang: eng
  text: Rab3 interacting molecules (RIMs) are highly enriched in the active zones
    of presynaptic terminals. It is generally thought that they operate as effectors
    of the small G protein Rab3. Three recent papers, by Han et al. (this issue of
    Neuron), Deng et al. (this issue of Neuron), and Kaeser et al. (a recent issue
    of Cell), shed new light on the functional role of RIM in presynaptic terminals.
    First, RIM tethers Ca2+ channels to active zones. Second, RIM contributes to priming
    of synaptic vesicles by interacting with another presynaptic protein, Munc13.
author:
- first_name: Alejandro
  full_name: Pernia-Andrade, Alejandro
  id: 36963E98-F248-11E8-B48F-1D18A9856A87
  last_name: Pernia-Andrade
- first_name: Peter M
  full_name: Jonas, Peter M
  id: 353C1B58-F248-11E8-B48F-1D18A9856A87
  last_name: Jonas
  orcid: 0000-0001-5001-4804
citation:
  ama: Pernia-Andrade A, Jonas PM. The multiple faces of RIM. <i>Neuron</i>. 2011;69(2):185-187.
    doi:<a href="https://doi.org/10.1016/j.neuron.2011.01.010">10.1016/j.neuron.2011.01.010</a>
  apa: Pernia-Andrade, A., &#38; Jonas, P. M. (2011). The multiple faces of RIM. <i>Neuron</i>.
    Elsevier. <a href="https://doi.org/10.1016/j.neuron.2011.01.010">https://doi.org/10.1016/j.neuron.2011.01.010</a>
  chicago: Pernia-Andrade, Alejandro, and Peter M Jonas. “The Multiple Faces of RIM.”
    <i>Neuron</i>. Elsevier, 2011. <a href="https://doi.org/10.1016/j.neuron.2011.01.010">https://doi.org/10.1016/j.neuron.2011.01.010</a>.
  ieee: A. Pernia-Andrade and P. M. Jonas, “The multiple faces of RIM,” <i>Neuron</i>,
    vol. 69, no. 2. Elsevier, pp. 185–187, 2011.
  ista: Pernia-Andrade A, Jonas PM. 2011. The multiple faces of RIM. Neuron. 69(2),
    185–187.
  mla: Pernia-Andrade, Alejandro, and Peter M. Jonas. “The Multiple Faces of RIM.”
    <i>Neuron</i>, vol. 69, no. 2, Elsevier, 2011, pp. 185–87, doi:<a href="https://doi.org/10.1016/j.neuron.2011.01.010">10.1016/j.neuron.2011.01.010</a>.
  short: A. Pernia-Andrade, P.M. Jonas, Neuron 69 (2011) 185–187.
date_created: 2018-12-11T12:02:56Z
date_published: 2011-01-27T00:00:00Z
date_updated: 2021-01-12T07:43:00Z
day: '27'
department:
- _id: PeJo
doi: 10.1016/j.neuron.2011.01.010
intvolume: '        69'
issue: '2'
language:
- iso: eng
month: '01'
oa_version: None
page: 185 - 187
publication: Neuron
publication_status: published
publisher: Elsevier
publist_id: '3243'
quality_controlled: '1'
scopus_import: 1
status: public
title: The multiple faces of RIM
type: journal_article
user_id: 4435EBFC-F248-11E8-B48F-1D18A9856A87
volume: 69
year: '2011'
...
---
_id: '3718'
abstract:
- lang: eng
  text: Long-term depression (LTD) is a form of synaptic plasticity that may contribute
    to information storage in the central nervous system. Here we report that LTD
    can be elicited in layer 5 pyramidal neurons of the rat prefrontal cortex by pairing
    low frequency stimulation with a modest postsynaptic depolarization. The induction
    of LTD required the activation of both metabotropic glutamate receptors of the
    mGlu1 subtype and voltage-sensitive Ca(2+) channels (VSCCs) of the T/R, P/Q and
    N types, leading to the stimulation of intracellular inositol trisphosphate (IP3)
    receptors by IP3 and Ca(2+). The subsequent release of Ca(2+) from intracellular
    stores activated the protein phosphatase cascade involving calcineurin and protein
    phosphatase 1. The activation of purinergic P2Y(1) receptors blocked LTD. This
    effect was prevented by P2Y(1) receptor antagonists and was absent in mice lacking
    P2Y(1) but not P2Y(2) receptors. We also found that activation of P2Y(1) receptors
    inhibits Ca(2+) transients via VSCCs in the apical dendrites and spines of pyramidal
    neurons. In addition, we show that the release of ATP under hypoxia is able to
    inhibit LTD by acting on postsynaptic P2Y(1) receptors. In conclusion, these data
    suggest that the reduction of Ca(2+) influx via VSCCs caused by the activation
    of P2Y(1) receptors by ATP is the possible mechanism for the inhibition of LTD
    in prefrontal cortex.
acknowledgement: " The financial support of the Deutsche Forschungsgemeinschaft (IL
  20/12-1, KI 677/2-4) is gratefully acknowledged.\r\nWe thank B. H. Koller (Department
  of Genetics and Molecular Biology, University of North Carolina at Chapel Hill,
  NC, USA) for the generous supply of P2Y1−/− and P2Y2−/− mice. We are grateful to
  Dr. A. Schulz for reanalysing the genotype of the P2Y1−/− mice. The authors thank
  P. Jonas and U. Heinemann for many helpful comments and A-K. Krause, L Feige and
  M. Eberts for their excellent technical support."
author:
- first_name: José
  full_name: Guzmán, José
  id: 30CC5506-F248-11E8-B48F-1D18A9856A87
  last_name: Guzmán
- first_name: Hartmut
  full_name: Schmidt, Hartmut
  last_name: Schmidt
- first_name: Heike
  full_name: Franke, Heike
  last_name: Franke
- first_name: Ute
  full_name: Krügel, Ute
  last_name: Krügel
- first_name: Jens
  full_name: Eilers, Jens
  last_name: Eilers
- first_name: Peter
  full_name: Illes, Peter
  last_name: Illes
- first_name: Zoltan
  full_name: Gerevich, Zoltan
  last_name: Gerevich
citation:
  ama: Guzmán J, Schmidt H, Franke H, et al. P2Y1 receptors inhibit long-term depression
    in the prefrontal cortex. <i>Neuropharmacology</i>. 2010;59(6):406-415. doi:<a
    href="https://doi.org/10.1016/j.neuropharm.2010.05.013">10.1016/j.neuropharm.2010.05.013</a>
  apa: Guzmán, J., Schmidt, H., Franke, H., Krügel, U., Eilers, J., Illes, P., &#38;
    Gerevich, Z. (2010). P2Y1 receptors inhibit long-term depression in the prefrontal
    cortex. <i>Neuropharmacology</i>. Elsevier. <a href="https://doi.org/10.1016/j.neuropharm.2010.05.013">https://doi.org/10.1016/j.neuropharm.2010.05.013</a>
  chicago: Guzmán, José, Hartmut Schmidt, Heike Franke, Ute Krügel, Jens Eilers, Peter
    Illes, and Zoltan Gerevich. “P2Y1 Receptors Inhibit Long-Term Depression in the
    Prefrontal Cortex.” <i>Neuropharmacology</i>. Elsevier, 2010. <a href="https://doi.org/10.1016/j.neuropharm.2010.05.013">https://doi.org/10.1016/j.neuropharm.2010.05.013</a>.
  ieee: J. Guzmán <i>et al.</i>, “P2Y1 receptors inhibit long-term depression in the
    prefrontal cortex.,” <i>Neuropharmacology</i>, vol. 59, no. 6. Elsevier, pp. 406–415,
    2010.
  ista: Guzmán J, Schmidt H, Franke H, Krügel U, Eilers J, Illes P, Gerevich Z. 2010.
    P2Y1 receptors inhibit long-term depression in the prefrontal cortex. Neuropharmacology.
    59(6), 406–415.
  mla: Guzmán, José, et al. “P2Y1 Receptors Inhibit Long-Term Depression in the Prefrontal
    Cortex.” <i>Neuropharmacology</i>, vol. 59, no. 6, Elsevier, 2010, pp. 406–15,
    doi:<a href="https://doi.org/10.1016/j.neuropharm.2010.05.013">10.1016/j.neuropharm.2010.05.013</a>.
  short: J. Guzmán, H. Schmidt, H. Franke, U. Krügel, J. Eilers, P. Illes, Z. Gerevich,
    Neuropharmacology 59 (2010) 406–415.
date_created: 2018-12-11T12:04:47Z
date_published: 2010-11-01T00:00:00Z
date_updated: 2021-01-12T07:51:42Z
day: '01'
department:
- _id: PeJo
doi: 10.1016/j.neuropharm.2010.05.013
intvolume: '        59'
issue: '6'
language:
- iso: eng
month: '11'
oa_version: None
page: 406 - 415
publication: Neuropharmacology
publication_status: published
publisher: Elsevier
publist_id: '2512'
quality_controlled: '1'
scopus_import: 1
status: public
title: P2Y1 receptors inhibit long-term depression in the prefrontal cortex.
type: journal_article
user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87
volume: 59
year: '2010'
...
