神经传递
长时程增强
荷包牡丹碱
加巴能
神经科学
抑制性突触后电位
氟西汀
突触后电位
海马结构
利坦西林
药理学
化学
γ-氨基丁酸受体
血清素
生物
5-羟色胺受体
受体
生物化学
作者
Zengyou Ye,Ke Zhou,Tian Xu,Jiang Zhou
标识
DOI:10.1016/j.neulet.2008.06.072
摘要
The GABA system is highly involved in the pathophysiology of mood disorders such as depression. Altered GABAergic function is evident in depressed patients and animal models of depression. Currently, the most widely used antidepressants are selective 5-HT reuptake inhibitors, such as fluoxetine. However, the effects of fluoxetine on GABAergic synaptic neurotransmission remain poorly investigated. Whole-cell patch-clamp recordings from cultured rat hippocampal neurons were therefore conducted to investigate the effects of fluoxetine on GABAergic neurotransmission. The spontaneous inhibitory postsynaptic current (sIPSC) was completely blocked by 10 microM bicuculline and reversibly potentiated by 30 microM fluoxetine. The fluoxetine potentiation on either amplitude or frequency of sIPSCs was dose-dependent, with the EC(50) values of 10.96 and 14.26 microM, respectively. This potentiation was also TTX-insensitive, suggesting independence of presynaptic action potentials. The ritanserin (5 microM), a selective 5-HT(2) receptor antagonist, did not alter the fluoxetine potentiation on miniature inhibitory postsynaptic currents. Taken together, our data suggest that fluoxetine can potentiate GABAergic neurotransmission without depending on presynaptic firing of action potentials and its elevating of 5-HT receptor activities. This potentiation by fluoxetine may normalize the hippocampal GABA deficit during depression and in part exert its antidepressant activity.
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