Specific GABAA Circuits for Visual Cortical Plasticity

Michela Fagiolini, Joan Marc Fritschy, Karin Löw, Hanns Möhler, Uwe Rudolph, Takao K. Hensch

Research output: Contribution to journalArticlepeer-review

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-minobutyric acid (GABA)-mediated transmission with benzodiazepines. Here, we use a mouse "knockin" mutation to α subunits that renders individual GABA type A (GABAA) 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.

Original languageEnglish (US)
Pages (from-to)1681-1683
Number of pages3
JournalScience
Volume303
Issue number5664
DOIs
StatePublished - Mar 12 2004
Externally publishedYes

ASJC Scopus subject areas

  • General

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