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

Cell Reports
Hongyu SunFrances E Jensen

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.

Citations

Sep 19, 2019·Nature Reviews. Neurology·Annabel K Short, Tallie Z Baram
Aug 9, 2020·Frontiers in Cellular Neuroscience·Weifeng XuOliver M Schlüter
Jan 31, 2019·Annual Review of Neuroscience·Andrej KralBlake S Wilson
May 2, 2019·Frontiers in Neuroanatomy·Patrick O KanoldXiangying Meng
Jun 7, 2020·Proceedings of the National Academy of Sciences of the United States of America·Rebecca K RehTakao K Hensch
Mar 3, 2021·Proceedings of the National Academy of Sciences of the United States of America·Rashad YusifovSiegrid Löwel
May 21, 2021·Molecular and Cellular Neurosciences·Jocelyn J Lippman-BellFrances E Jensen

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