NMDAR-dependent presynaptic homeostasis in adult hippocampus: Synapse growth and cross-modal inhibitory plasticity.

Autor:	Chipman PH; Department of Biochemistry and Biophysics, Kavli Institute for Fundamental Neuroscience, University of California, San Francisco, San Francisco, CA 94941, USA., Fetter RD; Department of Biochemistry and Biophysics, Kavli Institute for Fundamental Neuroscience, University of California, San Francisco, San Francisco, CA 94941, USA., Panzera LC; Department of Biological Sciences, Dartmouth College, Hanover, NH 03755, USA., Bergerson SJ; Department of Biological Sciences, Dartmouth College, Hanover, NH 03755, USA., Karmelic D; Department of Biochemistry and Biophysics, Kavli Institute for Fundamental Neuroscience, University of California, San Francisco, San Francisco, CA 94941, USA., Yokoyama S; Department of Biochemistry and Biophysics, Kavli Institute for Fundamental Neuroscience, University of California, San Francisco, San Francisco, CA 94941, USA., Hoppa MB; Department of Biological Sciences, Dartmouth College, Hanover, NH 03755, USA., Davis GW; Department of Biochemistry and Biophysics, Kavli Institute for Fundamental Neuroscience, University of California, San Francisco, San Francisco, CA 94941, USA. Electronic address: graeme.davis@ucsf.edu.
Jazyk:	angličtina
Zdroj:	Neuron [Neuron] 2022 Oct 19; Vol. 110 (20), pp. 3302-3317.e7. Date of Electronic Publication: 2022 Sep 06.
DOI:	10.1016/j.neuron.2022.08.014
Abstrakt:	Homeostatic plasticity (HP) encompasses a suite of compensatory physiological processes that counteract neuronal perturbations, enabling brain resilience. Currently, we lack a complete description of the homeostatic processes that operate within the mammalian brain. Here, we demonstrate that acute, partial AMPAR-specific antagonism induces potentiation of presynaptic neurotransmitter release in adult hippocampus, a form of compensatory plasticity that is consistent with the expression of presynaptic homeostatic plasticity (PHP) documented at peripheral synapses. We show that this compensatory plasticity can be induced within minutes, requires postsynaptic NMDARs, and is expressed via correlated increases in dendritic spine volume, active zone area, and docked vesicle number. Further, simultaneous postsynaptic genetic reduction of GluA1, GluA2, and GluA3 in triple heterozygous knockouts induces potentiation of presynaptic release. Finally, induction of compensatory plasticity at excitatory synapses induces a parallel, NMDAR-dependent potentiation of inhibitory transmission, a cross-modal effect consistent with the anti-epileptic activity of AMPAR-specific antagonists used in humans. Competing Interests: Declaration of interests G.W.D. is a member of the advisory board of the journal Neuron. (Copyright © 2022 The Author(s). Published by Elsevier Inc. All rights reserved.)
Databáze:	MEDLINE
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