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Publication : Inhibitory threshold for critical-period activation in primary visual cortex.

First Author  Fagiolini M Year  2000
Journal  Nature Volume  404
Issue  6774 Pages  183-6
PubMed ID  10724170 Mgi Jnum  J:112387
Mgi Id  MGI:3656189 Doi  10.1038/35004582
Citation  Fagiolini M, et al. (2000) Inhibitory threshold for critical-period activation in primary visual cortex. Nature 404(6774):183-6
abstractText  Neuronal circuits across several systems display remarkable plasticity to sensory input during postnatal development. Experience-dependent refinements are often restricted to well-defined critical periods in early life, but how these are established remains mostly unknown. A representative example is the loss of responsiveness in neocortex to an eye deprived of vision. Here we show that the potential for plasticity is retained throughout life until an inhibitory threshold is attained. In mice of all ages lacking an isoform of GABA (gamma-aminobutyric acid) synthetic enzyme (GAD65), as well as in immature wild-type animals before the onset of their natural critical period, benzodiazepines selectively reduced a prolonged discharge phenotype to unmask plasticity. Enhancing GABA-mediated transmission early in life rendered mutant animals insensitive to monocular deprivation as adults, similar to normal wild-type mice. Short-term presynaptic dynamics reflected a synaptic reorganization in GAD65 knockout mice after chronic diazepam treatment. A threshold level of inhibition within the visual cortex may thus trigger, once in life, an experience-dependent critical period for circuit consolidation, which may otherwise lie dormant.
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