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PubMed · 15017002

Specific GABAA circuits for visual cortical plasticity.

Michela Fagiolini·Jean-Marc Fritschy·Karin Löw·Hanns Möhler·Uwe Rudolph·Takao K Hensch
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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.

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AnimalsDiazepamDominance, OcularInterneuronsMiceMice, Inbred C57BLModels, NeurologicalMutationNeural InhibitionNeuronal PlasticityNeuronsProtein SubunitsPyridinesReceptors, GABA-ASynaptic TransmissionVision, OcularVisual CortexZolpidemgamma-Aminobutyric AcidJournal ArticleResearch Support, Non-U.S. Gov't

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Michela Fagiolini, Jean-Marc Fritschy, Karin Löw, Hanns Möhler, Uwe Rudolph, Takao K Hensch. 2004-03-12. Specific GABAA circuits for visual cortical plasticity.. https://doi.org/10.1126/science.1091032

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