Specific GABAA circuits for visual cortical plasticity
- PMID: 15017002
- DOI: 10.1126/science.1091032
Specific GABAA circuits for visual cortical plasticity
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 gamma-aminobutyric acid (GABA)-mediated transmission with benzodiazepines. Here, we use a mouse "knockin" mutation to alpha 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 alpha1-containing circuits were found to drive cortical plasticity, whereas alpha2-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.
Comment in
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Neuroscience. Blocking plasticity in the visual cortex.Science. 2004 Mar 12;303(5664):1619-21. doi: 10.1126/science.1096224. Science. 2004. PMID: 15016985 No abstract available.
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