Monocular deprivation (MD) during the critical period reduces the visual cortical response to the deprived eye and causes the geniculocortical axons serving the deprived eye to retract. When MD is combined with a pharmacological inhibition of the visual cortex, the cortical neurons weaken their response to an open eye and the input axons serving the open eye retract. To determine whether the 2 types of ocular dominance (OD) plasticity reflect an experience-driven modification of neural circuits sharing the same developmental time course, we analyzed the OD plasticity in an inhibited visual cortex using cats at different ages. MD did not affect the OD distribution in the inhibited cortex of adults, confirming that the OD plasticity in the inhibited cortex represents a developmental plasticity. In developing animals, the OD plasticity in the inhibited cortex was observed at the late phase of the critical period (P40-46) but not at the early phase (P22-26). We found a retraction of input axons serving an open eye at the late phase, whereas those at the early phase were comparable to the axons of normal animals. Therefore, the maturation of visual circuits might include an experience-driven rearrangement of thalamocortical projections during the late phase of development.
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