摘要

Activation of delta-opioid receptors (DOR) attenuates anoxic K leakage and protects cortical neurons from anoxic insults by inhibiting Na influx. It is unknown, however, which pathway(s) that mediates the Na influx is the target of DOR signal. In the present work, we found that, in the cortex, (1) DOR protection was largely dependent on the inhibition of anoxic Na influxes mediated by voltage-gated Na channels; (2) DOR activation inhibited Na influx mediated by ionotropic glutamate N-methyl-D-aspartate (NMDA) receptors, but not that by non-NMDA receptors, although both played a role in anoxic K derangement; and (3) DOR activation had little effect on Na /Ca2 exchanger-based response to anoxia. We conclude that DOR activation attenuates anoxic K derangement by restricting Na influx mediated by Na channels and NMDA receptors, and that non-NMDA receptors and Na /Ca2 exchangers, although involved in anoxic K derangement in certain degrees, are less likely the targets of DOR signal.

  • 出版日期2009-3