Wang S, Yang Q, Moller C J, Sharp F R, Haglid K G
Institute of Neurobiology, University of Göteborg, Sweden.
Pharmacol Toxicol. 1996 Sep;79(3):166-8. doi: 10.1111/j.1600-0773.1996.tb00262.x.
The present study examined whether eliprodil (SL 82.0715), an N-methyl-D-aspartate (NMDA) receptor antagonist acting on the polyamine sites induced expression of the 70 kDa heat shock protein (HSP70) in the rat brain. Whereas the NMDA channel blocker MK801 consistently induced HSP70 in posterior cingulate and retrosplenial cortices, eliprodil had no such effects even at the highest dose (50 mg/kg, intraperitoneally), supporting the idea that injury to the cerebrocortical neurones by NMDA receptor antagonists is probably related to specific sites of the receptor. Furthermore, eliprodil, given immediately after injection of MK801, blocked the effects of MK801 on HSP70. The result is discussed in terms of high affinity of eliprodil for the sigma receptor.
本研究检测了作用于多胺位点的N-甲基-D-天冬氨酸（NMDA）受体拮抗剂依利罗地（SL 82.0715）是否能诱导大鼠脑内70 kDa热休克蛋白（HSP70）的表达。NMDA通道阻滞剂MK801始终能在后扣带回和压后皮质诱导HSP70的产生，而依利罗地即使在最高剂量（50 mg/kg，腹腔注射）时也没有这种作用，这支持了NMDA受体拮抗剂对大脑皮质神经元的损伤可能与受体的特定部位有关的观点。此外，在注射MK801后立即给予依利罗地，可阻断MK801对HSP70的作用。根据依利罗地对σ受体的高亲和力对该结果进行了讨论。
