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Early Seizures Prematurely Unsilence Auditory Synapses to Disrupt Thalamocortical Critical Period Plasticity.

Abstract
Heightened neural excitability in infancy and childhood results in increased susceptibility to seizures. Such early-life seizures are associated with language deficits and autism that can result from aberrant development of the auditory cortex. Here, we show that early-life seizures disrupt a critical period (CP) for tonotopic map plasticity in primary auditory cortex (A1). We show that this CP is characterized by a prevalence of "silent," NMDA-receptor (NMDAR)-only, glutamate receptor synapses in auditory cortex that become "unsilenced" due to activity-dependent AMPA receptor (AMPAR) insertion. Induction of seizures prior to this CP occludes tonotopic map plasticity by prematurely unsilencing NMDAR-only synapses. Further, brief treatment with the AMPAR antagonist NBQX following seizures, prior to the CP, prevents synapse unsilencing and permits subsequent A1 plasticity. These findings reveal that early-life seizures modify CP regulators and suggest that therapeutic targets for early post-seizure treatment can rescue CP plasticity.
AuthorsHongyu Sun, Anne E Takesian, Ting Ting Wang, Jocelyn J Lippman-Bell, Takao K Hensch, Frances E Jensen
JournalCell reports (Cell Rep) Vol. 23 Issue 9 Pg. 2533-2540 (05 29 2018) ISSN: 2211-1247 [Electronic] United States
PMID29847785 (Publication Type: Journal Article, Research Support, N.I.H., Extramural, Research Support, Non-U.S. Gov't)
CopyrightCopyright © 2018 The Authors. Published by Elsevier Inc. All rights reserved.
Chemical References
  • Quinoxalines
  • Receptors, AMPA
  • 2,3-dioxo-6-nitro-7-sulfamoylbenzo(f)quinoxaline
Topics
  • Animals
  • Auditory Perception (physiology)
  • Cerebral Cortex (physiopathology)
  • Female
  • Male
  • Mice, Inbred C57BL
  • Neuronal Plasticity (physiology)
  • Quinoxalines (pharmacology)
  • Receptors, AMPA (antagonists & inhibitors, metabolism)
  • Seizures (physiopathology)
  • Synapses (physiology)
  • Thalamus (physiopathology)

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