CAJ | 학술논문

采用盲法膜片钳技术观察突触前烟碱受体(nicotinic acetylcholine receptors,nAChRs)对海马脑片CA1区锥体神经元兴奋性突触传递的调控作用.结果显示,nAChRs激动剂碘化二甲基苯基哌嗪(dimethylphenyl-piperazinium iodide,DMPP)不能在CA1区锥体神经元上诱发出烟碱电流.DMPP对CA1区锥体神经元自发兴奋性突触后电流(spontaneous excitatory postsynaptic current,sEPSC)具有明显的增频和增幅作用,并呈现明显的浓度依赖关系.DMPP对微小兴奋性突触后电流(miniature excitatory postsynaptic current,mEPSC)具有增频作用,但不具有增幅作用.上述DMPP增强突触传递的作用不能被nAChRs拮抗剂美加明、六烃季铵和双氢-β-刺桐丁所阻断,但可被α-银环蛇毒素阻断.上述结果提示,海马脑片CA1区锥体神经元兴奋性突触前nAChRs含有对α-银环蛇毒素敏感的α7亚单位,其激活可增强海马CA1区锥体神经元突触前递质谷氨酸的释放,从而对兴奋性突触传递发挥调控作用.
채용맹법막편겸기술관찰돌촉전연감수체(nicotinic acetylcholine receptors,nAChRs)대해마뇌편CA1구추체신경원흥강성돌촉전체적조공작용.결과현시,nAChRs격동제전화이갑기분기고진(dimethylphenyl-piperazinium iodide,DMPP)불능재CA1구추체신경원상유발출연감전류.DMPP대CA1구추체신경원자발흥강성돌촉후전류(spontaneous excitatory postsynaptic current,sEPSC)구유명현적증빈화증폭작용,병정현명현적농도의뢰관계.DMPP대미소흥강성돌촉후전류(miniature excitatory postsynaptic current,mEPSC)구유증빈작용,단불구유증폭작용.상술DMPP증강돌촉전체적작용불능피nAChRs길항제미가명、륙경계안화쌍경-β-자동정소조단,단가피α-은배사독소조단.상술결과제시,해마뇌편CA1구추체신경원흥강성돌촉전nAChRs함유대α-은배사독소민감적α7아단위,기격활가증강해마CA1구추체신경원돌촉전체질곡안산적석방,종이대흥강성돌촉전체발휘조공작용.
The effects of presynaptic nicotinic acetylcholine receptors (nAChRs) on excitatory synaptic transmission in CA1 pyramidal neurons of the rat hippocampus were examined by blind whole-cell patch clamp recording from hippocampal slice preparations. Local application of the nAChRs agonist dimethylphenyl-piperazinium iodide (DMPP) did not induce a postsynaptic current response in CA1 pyramidal cells. However, DMPP enhanced the frequency and amplitude of spontaneous excitatory postsynaptic current (sEPSC) in these cells in a dose-dependent manner. This enhancement was blocked by the selective nicotinic α-7 receptor antagonist α-bungarotoxin, but not by the antagonist mecamylamine, hexamethonium or dihyhro3-erythroidine. The frequency of miniature excitatory postsynaptic current (mEPSC) in CA1 pyramidal neurons was also increased by application of DMPP, indicating a presynaptic site of action of the agonist. Taken together, these results suggest that activation of presynaptic nAChRs in CA1 pyramidal neurons, which contain α-7 subunits, potentiates presynaptic glutamate release and consequently modulate excitatory synaptic transmission in the hippocampus.