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目的 研究皮质酮对海马神经元电压门控性钙通道和突触活动的影响 ,以阐明其作用机理。方法 以培养的新生大鼠海马神经元为标本 ,使用膜片钳技术的全细胞记录方式 ,通过压力注射给药的方法观察皮质酮对神经元电压门控性钙通道及其自发性突触活动的影响。结果 皮质酮 1、10和 10 0μmol·L- 1可使神经元电压门控性钙电流的幅度分别增加 (14± 8) %、(41± 13) %和 (5 8± 9) % ,其增强效应具有明显的浓度依赖性特征 ,但没有电压依赖性 ,也不改变钙通道的电学特征。 10 0 μmol·L- 1皮质酮可使海马神经元突触活动的发生频率增加约 4倍。在使用河豚毒素阻断神经元的突触传递活动后 ,皮质酮仍然可以诱发低频 (4.6± 1.0 )Hz低幅 (0 .18±0 .0 9)nA的兴奋性突触后电流。结论 皮质酮对海马神经元电压门控性钙电流及其突触活动有明显的增强作用。皮质酮的即刻增强效应可能与其调节基因表达的作用无关。
Objective To investigate the effects of corticosterone on voltage-gated calcium channel and synaptic activity in hippocampal neurons in order to clarify its mechanism. Methods The cultured hippocampal neurons of newborn rats were used as samples. The whole-cell recording method of patch clamp technique was used to observe the effect of corticosterone on voltage-gated calcium channel and its spontaneous synaptic activity Impact. Results Cortisone 1, 10 and 10 μmol·L -1 increased the amplitude of voltage-gated calcium currents in neurons by (14 ± 8)%, (41 ± 13)% and (58 ± 9)%, respectively The enhancement effect has obvious concentration-dependent characteristics, but no voltage dependence and does not change the electrical characteristics of calcium channel. Corticosterone at 10 0 μmol·L -1 increased the synaptic activity of hippocampal neurons by about 4-fold. After tetrodotoxin blocked neuronal synaptic transmission, corticosterone still induced excitatory postsynaptic currents in the low (.6 ± 1.0) Hz low amplitude (.18 ± 0.09) nA. Conclusion Corticosterone can significantly enhance the voltage-gated calcium current and synaptic activity in hippocampal neurons. The immediate enhancement of corticosterone may not be related to its role in regulating gene expression.