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背侧缝核是中枢神经系统中含 5 -羟色胺 (5 -HT)细胞最多的核团。早期的电生理研究表明 :这些细胞含有 5 -HT1A自受体 ,它可以偶联开放整合性钾通道和抑制性电压依赖性钙通道。这种 5 -HT对突触后 5 -HT自受体的直接作用对于调节 5 -HT神经元的放电有负反馈作用 ,但是从未见报道关于 5 -羟色胺通过局部突触活动调节自身功能。本实验的目的就在于探测 5 -HT如何通过突触电流调节自身功能 ,并且决定是那一种 5 -羟色胺受体亚型介导这种作用。用细胞内记录的方法 ,在鼠脑片我们观察到 5 -羟色胺可以浓度依赖性地增加 5 -HT神经元产生的自发的抑制性突触后电流 (IPSCs) ,这种作用可以被γ -氨基丁酸A(GABA)受体拮抗剂bicuculline完全阻断 ,也可以被快钠通道阻断剂TTX阻断。表明 5 -HT可以通过兴奋GABA能神经元抑制背侧缝核 5 -HT神经元的活动。进一步我们探测了共受体亚型 ,发现 5 -HT引起的这种抑制性突触后电流可以被一种 5 -HT2 受体拮抗剂MDI - 10 0 90 7(30nmol/L ,2 5min)阻断。表明 5 -HT通过 5 -HT2A受体兴奋GABAA 能神经元 ,继而释放GABA结合于 5 -HT神经元的GABAA 受体 ,产生抑制性突触后电流 ,达到局部负反馈调节的作用。
The dorsal raphe nucleus is the nucleus with the most 5-HT (5-HT) cells in the central nervous system. Early electrophysiological studies showed that these cells contain the 5-HT1A auto-receptor, which can be coupled to open up an integrated potassium channel and an inhibitory voltage-dependent calcium channel. This direct effect of 5-HT on post-synaptic 5-HT self-receptors has a negative feedback effect on the regulation of 5-HT neuronal discharge, but no reports have been reported about the regulatory function of serotonin through local synaptic activity. The purpose of this experiment was to probe how 5-HT regulates its function through synaptic currents and determines which 5-HT receptor subtype mediates this effect. Using intracellular recordings, we observed in rat brain slices that serotonin can increase the spontaneous inhibitory postsynaptic currents (IPSCs) produced by 5-HT neurons in a concentration-dependent manner, which can be blocked by γ-amino The bicuculline, a butyric acid (GABA) receptor antagonist, is completely blocked and can also be blocked by the fast sodium channel blocker TTX. This indicates that 5-HT can inhibit the activity of dorsal karyopyon 5-HT neurons by excitement of GABAergic neurons. Further, we detected co-receptor subtypes and found that this inhibitory post-synaptic current induced by 5-HT was blocked by a 5-HT2 receptor antagonist MDI-10 0 907 (30 nmol / L, 25 min) Off. It shows that 5-HT excites GABAAergic neurons via 5-HT2A receptor and then releases GABA to GABAA receptor of 5-HT neurons to produce inhibitory postsynaptic currents and achieve local negative feedback regulation.