Rapid effect of stress concentration corticosterone on glutamate receptor and its subtype NMDA receptor activity in cultured hippocampal neurons

Objective: To study the rapid effect of glucocorticoids (GCs) on NMDA receptor activity in hippocampal neurons in stress and to elucidate its underlying probable membrane mechanisms. Methods: Whole-cell patch-clamp recording was used to assess the effect of stress concentration corticosterone (B) on the responses of cultured hippocampal neurons to glutamate and NMDA (N-methy-D-asparatic acid). To make clear the target of B, intracellular dialysis of B(10 μmol/L)through patch pipette and extracellular application of bovine serum albumin-conjugated corticosterone(B-BSA, 10 μmol/L)were carried out to observe their influence on peak amplitude of NMDA-evoked current. Results: B had a rapid, reversible and inhibitory effect on peak amplitude of GLU- or NMDA-evoked current in cultured hippocampal neurons. Furthermore, B-BSA had the inhibitory effect on INMDA as that of B, but intracellularly dialyzed B had no significant effect on I NMDA. Conclusion: These results suggest that under the condition of stress, GCs may rapidly, negatively regulate excitatory synaptic receptors-glutamate receptors (GluRs), especially NMDA receptor (NMDAR) in central nervous system, which is mediated by rapid membrane mechanisms, but not by classical, genomic mechanisms.