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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-piperazini-um 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-B-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。
Blind patch clamp technique was used to observe the regulatory effect of nicotinic acetylcholine receptors (nAChRs) on excitatory synaptic transmission in CA1 pyramidal neurons of hippocampal slices. The results showed that NAChRs agonist dimethylphenyl-piperazini-um iodide (DMPP) failed to induce nicotinic currents in CA1 pyramidal neurons. DMPP can significantly increase and increase spontaneous excitatory postsynaptic currents (CAPSE) in CA1 pyramidal neurons, and show a significant concentration-dependent relationship. DMPP has a frequency-increasing effect on miniature excitatory postsynaptic currents (mEPSC) but does not have an amplifying effect. The above-mentioned effects of DMPP-enhanced synaptic transmission can not be blocked by the nAChRs antagonists mecamylamine, hexaalkyldimethylammonium and dihydro-B-spatin but are blocked by alpha-bungarotoxin. These results suggest that hippocampal CA1 pyramidal neurons in the excitatory synaptic nAChRs contain α-bungarotoxin-sensitive α7 subunit, the activation can increase the pyramidal neurons in the hippocampal CA1 pyramidal neurotransmitter Valley The release of amino acids, which play a regulatory role of excitatory synaptic transmission.