Regulation of ERK phosphorylation by ethanol in fetal cortical neurons.

摘要

Using fetal cortical neurons and phospho-specific MAP kinase antibody, we investigated the modulation of MAP kinase pathway by ethanol. Our results show that acute ethanol inhibited, while chronic treatment increased, the phosphorylation of MAP kinase per se; likewise AP-5 (a competitive antagonist for NMDA receptors) also increased the basal phosphorylation of MAP kinase following chronic treatment for 5 days. However, chronic ethanol or AP-5 induced MAP kinase phosphorylation was inhibited by KN-62 (calcium calmodulin dependent kinase inhibitor), suggesting the possible involvement of CaM (Calcium calmodulin) kinase. Immunoblot analysis revealed an upregulation of CaM kinase content in chronic ethanol and AP-5 treated cells. These results indicate that acute ethanol may inhibit, while chronic ethanol treatment increases, the basal phosphorylation of MAP kinase per se.