@article{8674, abstract = {Extrasynaptic actions of glutamate are limited by high-affinity transporters expressed by perisynaptic astroglial processes (PAPs): this helps maintain point-to-point transmission in excitatory circuits. Memory formation in the brain is associated with synaptic remodeling, but how this affects PAPs and therefore extrasynaptic glutamate actions is poorly understood. Here, we used advanced imaging methods, in situ and in vivo, to find that a classical synaptic memory mechanism, long-term potentiation (LTP), triggers withdrawal of PAPs from potentiated synapses. Optical glutamate sensors combined with patch-clamp and 3D molecular localization reveal that LTP induction thus prompts spatial retreat of astroglial glutamate transporters, boosting glutamate spillover and NMDA-receptor-mediated inter-synaptic cross-talk. The LTP-triggered PAP withdrawal involves NKCC1 transporters and the actin-controlling protein cofilin but does not depend on major Ca2+-dependent cascades in astrocytes. We have therefore uncovered a mechanism by which a memory trace at one synapse could alter signal handling by multiple neighboring connections.}, author = {Henneberger, Christian and Bard, Lucie and Panatier, Aude and Reynolds, James P. and Kopach, Olga and Medvedev, Nikolay I. and Minge, Daniel and Herde, Michel K. and Anders, Stefanie and Kraev, Igor and Heller, Janosch P. and Rama, Sylvain and Zheng, Kaiyu and Jensen, Thomas P. and Sanchez-Romero, Inmaculada and Jackson, Colin J. and Janovjak, Harald L and Ottersen, Ole Petter and Nagelhus, Erlend Arnulf and Oliet, Stephane H.R. and Stewart, Michael G. and Nägerl, U. VAlentin and Rusakov, Dmitri A. }, issn = {10974199}, journal = {Neuron}, number = {5}, pages = {P919--936.E11}, publisher = {Elsevier}, title = {{LTP induction boosts glutamate spillover by driving withdrawal of perisynaptic astroglia}}, doi = {10.1016/j.neuron.2020.08.030}, volume = {108}, year = {2020}, } @article{7684, author = {Gridchyn, Igor and Schönenberger, Philipp and O'Neill, Joseph and Csicsvari, Jozsef L}, issn = {10974199}, journal = {Neuron}, number = {2}, pages = {291--300.e6}, publisher = {Elsevier}, title = {{Assembly-specific disruption of hippocampal replay leads to selective memory deficit}}, doi = {10.1016/j.neuron.2020.01.021}, volume = {106}, year = {2020}, } @article{6830, author = {Contreras, Ximena and Hippenmeyer, Simon}, issn = {10974199}, journal = {Neuron}, number = {5}, pages = {750--752}, publisher = {Elsevier}, title = {{Memo1 tiles the radial glial cell grid}}, doi = {10.1016/j.neuron.2019.08.021}, volume = {103}, year = {2019}, } @article{944, abstract = {The concerted production of neurons and glia by neural stem cells (NSCs) is essential for neural circuit assembly. In the developing cerebral cortex, radial glia progenitors (RGPs) generate nearly all neocortical neurons and certain glia lineages. RGP proliferation behavior shows a high degree of non-stochasticity, thus a deterministic characteristic of neuron and glia production. However, the cellular and molecular mechanisms controlling RGP behavior and proliferation dynamics in neurogenesis and glia generation remain unknown. By using mosaic analysis with double markers (MADM)-based genetic paradigms enabling the sparse and global knockout with unprecedented single-cell resolution, we identified Lgl1 as a critical regulatory component. We uncover Lgl1-dependent tissue-wide community effects required for embryonic cortical neurogenesis and novel cell-autonomous Lgl1 functions controlling RGP-mediated glia genesis and postnatal NSC behavior. These results suggest that NSC-mediated neuron and glia production is tightly regulated through the concerted interplay of sequential Lgl1-dependent global and cell intrinsic mechanisms.}, author = {Beattie, Robert J and Postiglione, Maria P and Burnett, Laura and Laukoter, Susanne and Streicher, Carmen and Pauler, Florian and Xiao, Guanxi and Klezovitch, Olga and Vasioukhin, Valeri and Ghashghaei, Troy and Hippenmeyer, Simon}, issn = {08966273}, journal = {Neuron}, number = {3}, pages = {517 -- 533.e3}, publisher = {Cell Press}, title = {{Mosaic analysis with double markers reveals distinct sequential functions of Lgl1 in neural stem cells}}, doi = {10.1016/j.neuron.2017.04.012}, volume = {94}, year = {2017}, } @article{991, abstract = {Synaptotagmin 7 (Syt7) was originally identified as a slow Ca2+ sensor for lysosome fusion, but its function at fast synapses is controversial. The paper by Luo and Südhof (2017) in this issue of Neuron shows that at the calyx of Held in the auditory brainstem Syt7 triggers asynchronous release during stimulus trains, resulting in reliable and temporally precise high-frequency transmission. Thus, a slow Ca2+ sensor contributes to the fast signaling properties of the calyx synapse.}, author = {Chen, Chong and Jonas, Peter M}, issn = {08966273}, journal = {Neuron}, number = {4}, pages = {694 -- 696}, publisher = {Elsevier}, title = {{Synaptotagmins: That’s why so many}}, doi = {10.1016/j.neuron.2017.05.011}, volume = {94}, year = {2017}, } @article{2241, abstract = {The brain demands high-energy supply and obstruction of blood flow causes rapid deterioration of the healthiness of brain cells. Two major events occur upon ischemia: acidosis and liberation of excess glutamate, which leads to excitotoxicity. However, cellular source of glutamate and its release mechanism upon ischemia remained unknown. Here we show a causal relationship between glial acidosis and neuronal excitotoxicity. As the major cation that flows through channelrhodopsin-2 (ChR2) is proton, this could be regarded as an optogenetic tool for instant intracellular acidification. Optical activation of ChR2 expressed in glial cells led to glial acidification and to release of glutamate. On the other hand, glial alkalization via optogenetic activation of a proton pump, archaerhodopsin (ArchT), led to cessation of glutamate release and to the relief of ischemic brain damage in vivo. Our results suggest that controlling glial pH may be an effective therapeutic strategy for intervention of ischemic brain damage.}, author = {Beppu, Kaoru and Sasaki, Takuya and Tanaka, Kenji and Yamanaka, Akihiro and Fukazawa, Yugo and Shigemoto, Ryuichi and Matsui, Ko}, issn = {08966273}, journal = {Neuron}, number = {2}, pages = {314 -- 320}, publisher = {Elsevier}, title = {{Optogenetic countering of glial acidosis suppresses glial glutamate release and ischemic brain damage}}, doi = {10.1016/j.neuron.2013.11.011}, volume = {81}, year = {2014}, } @article{2254, abstract = {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 = {Pernia-Andrade, Alejandro and Jonas, Peter M}, issn = {08966273}, journal = {Neuron}, number = {1}, pages = {140 -- 152}, publisher = {Elsevier}, title = {{Theta-gamma-modulated synaptic currents in hippocampal granule cells in vivo define a mechanism for network oscillations}}, doi = {10.1016/j.neuron.2013.09.046}, volume = {81}, year = {2014}, }