Shibata S, Yamamoto Y, Watanabe S
Department of Pharmacology, Faculty of Pharmaceutical Sciences, Kyushu University 62, Fukuoka, Japan.
Brain Res. 1995 Jan 30;670(2):337-41. doi: 10.1016/0006-8993(94)01358-o.
Effects of sigma receptor agonists or antagonists on hypoxia/hypoglycemia-induced decrease in CA1 presynaptic fiber spikes elicited by the stimulation of Schaffer collaterals were investigated using rat hippocampal slices. Treatment with sigma receptor antagonists such as haloperidol, NE-100 and rimcazole produced a concentration-dependent attenuation of the hypoxia/hypoglycemia-induced decrease in CA1 presynaptic fiber spikes. The order of potency of protection against hypoxia/hypoglycemia-induced reduction in CA1 presynaptic potential was: NE-100 = haloperidol > rimcazole. Treatment with sigma receptor agonist DTG potentiated the hypoxia/hypoglycemia-induced decrease in the CA1 presynaptic potential, whereas SKF10047 which possesses an affinity for phencyclidine site attenuated the decrease of potential. NE-100 antagonized a functional deficit induced by DTG, but unaffected the improving effect induced by SKF10047. The present results suggest a facilitatory role of sigma receptor stimulation in hypoxia/hypoglycemia-induced an impairment of neurophysiological functions in CA1 presynaptic regions of hippocampal slices.
使用大鼠海马切片研究了σ受体激动剂或拮抗剂对缺氧/低血糖诱导的由刺激Schaffer侧支引起的CA1突触前纤维峰电位降低的影响。用σ受体拮抗剂如氟哌啶醇、NE-100和利木唑处理可产生浓度依赖性地减轻缺氧/低血糖诱导的CA1突触前纤维峰电位降低。对缺氧/低血糖诱导的CA1突触前电位降低的保护效力顺序为：NE-100 =氟哌啶醇>利木唑。用σ受体激动剂DTG处理可增强缺氧/低血糖诱导的CA1突触前电位降低，而对苯环利定位点具有亲和力的SKF10047可减轻电位降低。NE-100拮抗DTG诱导的功能缺陷，但不影响SKF10047诱导的改善作用。目前的结果表明，σ受体刺激在缺氧/低血糖诱导的海马切片CA1突触前区域神经生理功能损害中起促进作用。
