The mammalian visual system exhibits significant experience-induced plasticity in the early postnatal period. While physiological studies have revealed the contribution of the CB1 cannabinoid receptor (CB1) to developmental plasticity in the primary visual cortex (V1), it remains unknown whether the expression and localization of CB1 is regulated during development or by visual experience. To explore a possible role of the endocannabinoid system in visual cortical plasticity, we examined the expression of CB1 in the visual cortex of mice. We found intense CB1 immunoreactivity in layers II/III and VI. CB1 mainly localized at vesicular GABA transporter-positive inhibitory nerve terminals. The amount of CB1 protein increased throughout development, and the specific laminar pattern of CB1 appeared at P20 and remained until adulthood. Dark rearing from birth to P30 decreased the amount of CB1 protein in V1 and altered the synaptic localization of CB1 in the deep layer. Dark rearing until P50, however, did not influence the expression of CB1. Brief monocular deprivation for 2 days upregulated the localization of CB1 at inhibitory nerve terminals in the deep layer. Taken together, the expression and the localization of CB1 are developmentally regulated, and both parameters are influenced by visual experience.
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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