<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Quast KB</submitter><funding>MEXT | Japan Society for the Promotion of Science</funding><funding>HHS | National Institutes of Health</funding><funding>HHS | NIH | National Institute of Mental Health</funding><funding>NHLBI NIH HHS</funding><funding>NIMH NIH HHS</funding><funding>National Science Foundation</funding><pagination>e2123182120</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC9926253</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>120(2)</volume><pubmed_abstract>Early-life experience enduringly sculpts thalamocortical (TC) axons and sensory processing. Here, we identify the very first synaptic targets that initiate critical period plasticity, heralded by altered cortical oscillations. Monocular deprivation (MD) acutely induced a transient (&lt;3 h) peak in EEG γ-power (~40 Hz) specifically within the visual cortex, but only when the critical period was open (juvenile mice or adults after dark-rearing, &lt;i>Lynx1&lt;/i>-deletion, or diazepam-rescued GAD65-deficiency). Rapid TC input loss onto parvalbumin-expressing (PV) inhibitory interneurons (but not onto nearby pyramidal cells) was observed within hours of MD in a TC slice preserving the visual pathway - again once critical periods opened. Computational TC modeling of the emergent γ-rhythm in response t</pubmed_abstract><journal>Proceedings of the National Academy of Sciences of the United States of America</journal><pubmed_title>Rapid synaptic and gamma rhythm signature of mouse critical period plasticity.</pubmed_title><pmcid>PMC9926253</pmcid><funding_grant_id>1P0MH094271</funding_grant_id><funding_grant_id>T32 HL007901</funding_grant_id><funding_grant_id>5T32HL007901</funding_grant_id><funding_grant_id>WPI-IRCN</funding_grant_id><funding_grant_id>DGE0946799 DGE1144152</funding_grant_id><funding_grant_id>P50 MH094271</funding_grant_id><pubmed_authors>Quast KB</pubmed_authors><pubmed_authors>Hensch TK</pubmed_authors><pubmed_authors>Reh RK</pubmed_authors><pubmed_authors>Kopell N</pubmed_authors><pubmed_authors>McCarthy MM</pubmed_authors><pubmed_authors>Caiati MD</pubmed_authors></additional><is_claimable>false</is_claimable><name>Rapid synaptic and gamma rhythm signature of mouse critical period plasticity.</name><description>Early-life experience enduringly sculpts thalamocortical (TC) axons and sensory processing. Here, we identify the very first synaptic targets that initiate critical period plasticity, heralded by altered cortical oscillations. Monocular deprivation (MD) acutely induced a transient (&lt;3 h) peak in EEG γ-power (~40 Hz) specifically within the visual cortex, but only when the critical period was open (juvenile mice or adults after dark-rearing, &lt;i>Lynx1&lt;/i>-deletion, or diazepam-rescued GAD65-deficiency). Rapid TC input loss onto parvalbumin-expressing (PV) inhibitory interneurons (but not onto nearby pyramidal cells) was observed within hours of MD in a TC slice preserving the visual pathway - again once critical periods opened. Computational TC modeling of the emergent γ-rhythm in response t</description><dates><release>2023-01-01T00:00:00Z</release><publication>2023 Jan</publication><modification>2025-04-21T22:12:44.202Z</modification><creation>2025-04-21T22:12:44.202Z</creation></dates><accession>S-EPMC9926253</accession><cross_references><pubmed>36598942</pubmed><doi>10.1073/pnas.2123182120</doi></cross_references></HashMap>