在中枢神经系统(central nervous system,CNS)中,锌离子对配体门控型离子通道具有重要的调节作用。锌离子随着神经元的活动从突触前膜的囊泡中释放到突触间隙,对突触内受体进行调控。锌离子抑制N-甲基-D-天冬氨酸(N-methyl-D-aspartate,NMDA)型谷氨酸受体的活性,而对非NMDA型谷氨酸受体的调控具有多样性。由γ氨基丁酸(γ-aminobutyric acid,GABA)受体所介导的抑制性突触传递活动也受到锌离子的抑制;而锌离子对glycine受体则呈现出浓度依赖的双向调节效应。病理条件下,锌离子参与了兴奋性细胞毒作用所触发的神经元凋亡过程。本文主要阐述了在CNS中,锌离子对配体门控型离子通道所介导的突触传递活动的调控作用,以及这些调控作用的生理功能和病理意义。
In the central nervous system(CNS),zinc has a modulatory role of the ligand-gated ion channels. This divalent cation is released from presynaptic vesicles into the synaptic cleft upon neuronal activity and acts as a modulator of many ligand-gated ion channels.The NMDA-type glutamate receptors are inhibited by zinc,whereas non-NMDA type glutamate receptors appear to be differently affected.Furthermore,inhibitory transmission mediated via GABA receptors could be suppressed by zinc;however,zinc may bidirectionally modulate glycinergic transmission in a dose-dependent way.In pathological conditions,zinc effect also contributes to the excitotoxicity-induced neuronal death.Taken together,this review highlights the putative roles for zinc involved in the synaptic transmissions mediated by the ligand-gated ion channels in the CNS. Furthermore,the physiological and pathological roles of the zinc modulation are also discussed in this review.