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Abstract:
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 (CP) in early life, but how these are
established remains largely unknown. A representative example is
the loss of responsiveness in neocortex to an eye deprived of
vision. We have recently identified an animal model with a
reversible impairment in this ocular dominance plasticity. Here, we
show that the potential for plasticity is retained throughout life
as long as it is not expressed. In mice of all ages lacking an
isoform of GABA synthetic enzyme (GAD65), as well as immature wild
type animals prior to onset of their natural CP, benzodiazepines
selectively reduced a prolonged discharge phenotype to unmask
plasticity. Enhancing GABAergic transmission early in life rendered
mutant animals insensitive to monocular deprivation as adults,
similar to normal wild type mice. Postnatal insertion of the NR2A
subunit into NMDA receptors, however, was not necessary for
expressing a CP. An optimal inhibitory threshold within visual
cortex may thus trigger - once in life - an experience-dependent CP
for circuit consolidation, which may otherwise lie dormant.
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