Visual input regulates the activity of extracellular signal-regulated kinase 1/2 in the developing visual cortex

Abstract

Activity-dependent plasticity of ocular dominance in the primary visual cortex is one of the best-studied examples of plasticity in the critical period of developing brain. Although a variety of molecules are suggested to contribute to the plasticity, it is still not clear why visual cortex expresses high plasticity only in a short period called critical period. Recently it was reported that extracellular signal-regulated kinase 1/2 (ERK 1/2) is necessary in the ocular dominance plasticity. If ERK 1/2 is involved in the mechanism of this plasticity, visual deprivation would change the activity of ERK 1/2 during the critical period. To test this possibility, we examined effects of monocular deprivation on the phosphorylated ERK 1/2 proteins in the rat visual cortex by immunohistochemistry. Phospho-ERK 1/2 immunopositive cells were found mainly in layer 2/3 of the visual cortex. We found a significant decrease in number of phospho-ERK 1/2 immunopositive cells in animals deprived of vision. The reduction of phospho-ERK 1/2 immunopositive cells were more prominent in the cortical area receiving more inputs from the deprived eye. Moreover similar changes were observed in adult rats. These observations suggest that ERK 1/2 activation might contribute to plasticity in young rats, but its activation by visual inputs is not a critical period-specific event. The timing of critical period might be regulated by other mechanism. [Jpn J Physiol 54 Suppl:S165 (2004)]