Specific GABAA Circuits for Visual Cortical Plasticity

See allHide authors and affiliations

Science  12 Mar 2004:
Vol. 303, Issue 5664, pp. 1681-1683
DOI: 10.1126/science.1091032

You are currently viewing the abstract.

View Full Text


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 (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.

View Full Text