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Glucocorticoid (GC) acts through both genomic and nongenomic mechanisms. It affects the structure and function of the central nervous system, especially the hippocampus. Here we report an in vitro culture system that can yield embryonic hippocampal neurons deficient in the expression of GC receptor as demonstrated by immunoblotting, immunocytochemistry, and RT-PCR. Owing to this unique feature, those neuron preparations can serve as an ideal model for studying the nongenomic actions of GC on neural cells. In this study, we found that the Erk1/2, c-Jun N-terminal kinase (JNK), and p38 MAPKs were activated in these neurons by BSA-conjugated corticosterone within 15 min of treatment. This activation was not blocked by RU38486, spironolactone, or cycloheximide. Therefore, it is concluded that the activation of MAPKs observed here was due to the nongenomic action of GC. Furthermore, a 24-h incubation with corticosterone at concentrations ranged from 10(-11)-10(-5) M did not have an effect on the viability of GC receptor-deficient neurons.

endocrinology

Cultured Embryonic Hippocampal Neurons Deficient in Glucocorticoid (GC) Receptor: A Novel Model for Studying Nongenomic Effects of GC in the Neural System