TY - JOUR AU - Gridchyn, Igor AU - Schönenberger, Philipp AU - O'Neill, Joseph AU - Csicsvari, Jozsef L ID - 7684 IS - 2 JF - Neuron SN - 08966273 TI - Assembly-specific disruption of hippocampal replay leads to selective memory deficit VL - 106 ER - TY - JOUR AB - Post-tetanic potentiation (PTP) is an attractive candidate mechanism for hippocampus-dependent short-term memory. Although PTP has a uniquely large magnitude at hippocampal mossy fiber-CA3 pyramidal neuron synapses, it is unclear whether it can be induced by natural activity and whether its lifetime is sufficient to support short-term memory. We combined in vivo recordings from granule cells (GCs), in vitro paired recordings from mossy fiber terminals and postsynaptic CA3 neurons, and “flash and freeze” electron microscopy. PTP was induced at single synapses and showed a low induction threshold adapted to sparse GC activity in vivo. PTP was mainly generated by enlargement of the readily releasable pool of synaptic vesicles, allowing multiplicative interaction with other plasticity forms. PTP was associated with an increase in the docked vesicle pool, suggesting formation of structural “pool engrams.” Absence of presynaptic activity extended the lifetime of the potentiation, enabling prolonged information storage in the hippocampal network. AU - Vandael, David H AU - Borges Merjane, Carolina AU - Zhang, Xiaomin AU - Jonas, Peter M ID - 8001 IS - 3 JF - Neuron SN - 0896-6273 TI - Short-term plasticity at hippocampal mossy fiber synapses is induced by natural activity patterns and associated with vesicle pool engram formation VL - 107 ER - TY - JOUR AB - 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. AU - Henneberger, Christian AU - Bard, Lucie AU - Panatier, Aude AU - Reynolds, James P. AU - Kopach, Olga AU - Medvedev, Nikolay I. AU - Minge, Daniel AU - Herde, Michel K. AU - Anders, Stefanie AU - Kraev, Igor AU - Heller, Janosch P. AU - Rama, Sylvain AU - Zheng, Kaiyu AU - Jensen, Thomas P. AU - Sanchez-Romero, Inmaculada AU - Jackson, Colin J. AU - Janovjak, Harald L AU - Ottersen, Ole Petter AU - Nagelhus, Erlend Arnulf AU - Oliet, Stephane H.R. AU - Stewart, Michael G. AU - Nägerl, U. VAlentin AU - Rusakov, Dmitri A. ID - 8674 IS - 5 JF - Neuron SN - 08966273 TI - LTP induction boosts glutamate spillover by driving withdrawal of perisynaptic astroglia VL - 108 ER - TY - JOUR AU - Contreras, Ximena AU - Hippenmeyer, Simon ID - 6830 IS - 5 JF - Neuron SN - 08966273 TI - Memo1 tiles the radial glial cell grid VL - 103 ER -