Abstract

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.

Highlights

  • Experiences during early postnatal life play an important role in the development of brain function and the refinement of specific neural connections

  • We examined the postnatal development of protein expression, layer distribution, and synaptic localization of CB1 in the mouse V1, along with the effect of visual experience on these factors

  • We found that (i) intense CB1 immunoreactivity is mainly observed in layers II/III and VI and localizes at the vesicular GABA transporter (VGAT)

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Summary

Introduction

Experiences during early postnatal life play an important role in the development of brain function and the refinement of specific neural connections. Monocular deprivation (MD) in early postnatal life induces a significant loss of visual cortical responses to the deprived eye in the primary visual cortex (V1) [1,2]. This so-called ocular dominance plasticity (ODP) exhibits a critical period [2,3], a postnatal time window in which animals are susceptible to MD, and has been studied as a model of experience-dependent development of neural circuits. CB1 cannabinoid receptor (CB1) which localizes at presynaptic terminals is a major cannabinoid receptor in the central nervous system, and 2-arachidonoylglycerol is a major eCB that is synthesized by diacylglycerol lipase-aat postsynaptic sites [11,12]

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