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• W2002095654 abstract "Weak inhibition within visual cortex early in life prevents experience-dependent plasticity. Loss of responsiveness to an eye deprived of vision can be initiated prematurely by enhancing γ-aminobutyric acid (GABA)–mediated transmission with benzodiazepines. Here, we use a mouse “knockin” mutation to α subunits that renders individual GABA type A (GABA A ) receptors insensitive to diazepam to show that a particular inhibitory network controls expression of the critical period. Only α1-containing circuits were found to drive cortical plasticity, whereas α2-enriched connections separately regulated neuronal firing. This dissociation carries implications for models of brain development and the safe design of benzodiazepines for use in infants." @default.
• W2002095654 created "2016-06-24" @default.
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• W2002095654 date "2004-03-12" @default.
• W2002095654 modified "2023-10-11" @default.
• W2002095654 title "Specific GABA _A Circuits for Visual Cortical Plasticity" @default.
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• W2002095654 doi "https://doi.org/10.1126/science.1091032" @default.
• W2002095654 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/15017002" @default.
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