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目的:观察allopregnanolone与γ氨基丁酸(GABA)对兴奋性毒性的作用.方法:对原代培养大鼠大脑的皮层细胞,采用kainate(KA)处理,诱发兴奋性毒性.通过测定释放至细胞培养基中的乳酸盐脱氢酶(LDH)活性。观察allopregna-nolone与GABA对兴奋性毒性的作用.结果:短期 或长期KA处理,均增加 LDH活性的释放,其作用呈剂量依赖性,EC_(50)值分别为(0.16±0.03)mol/L和(0.257±0.15)mmol/L.短期(3 h)allopreg-nanolone (10-1000 nmol/L)处理对0.2 mmol/L KA诱导的 LDH活性的释放无明显影响.而长期(24 h)allopregnanolone(10-1000 nmol/L)处理抑制KA诱导的LDH活性的释放,其作用呈剂量依赖性,EC_(50)值为(436±19)nmol/L.短期GABA(0.1-100μmo 1/L)处理,加剧KA(0.2 mmol/L)诱导的 LDH活性的释放,其作用呈剂量依赖性,EC_(50)值为(2.7±1.0)μmol/L.长期GABA处理,对KA诱导的LDH活性的释放无明显影响.结论;allopregnanolone和 GABA对KA诱导的兴奋性毒性有不同作用.
OBJECTIVE: To observe the effect of allopregnanolone and gamma-aminobutyric acid (GABA) on excitotoxicity.Methods: Kainate (KA) -induced excitotoxicity was induced in primary cultured rat cortical cells, and then released to cell culture Lactate dehydrogenase (LDH) activity in the base. The effect of allopregna-nolone and GABA on excitotoxicity was observed.RESULTS: Both short-term and long-term KA treatment increased LDH release in a dose-dependent manner with EC50 values of (0.16 ± 0.03) mol / L And (0.257 ± 0.15) mmol / L allopreg-nanolone (10-1000 nmol / L) for short time (3 h) had no significant effect on the release of LDH induced by 0.2 mmol / (10-1000 nmol / L) inhibited KA-induced release of LDH activity in a dose-dependent manner with an EC50 value of (436 ± 19) nmol / L. Short-term GABA (0.1-100 μmol / Treatment, exacerbating the release of LDH induced by KA (0.2 mmol / L) in a dose-dependent manner with an EC 50 value of (2.7 ± 1.0) μmol / L. Long-term GABA treatment induced KA-induced LDH activity Release had no significant effect.Conclusion; allopregnanolone and GABA have different effects on KA-induced excitotoxicity.