Functional interconnection between cholinergic and peptidergic neurons in bullfrog sympathetic ganglia

药理学研究先前已报道了烟碱和肽能递质物质之间相互作用诱导的胆碱能传递的调节。然而，实验结果之间存在相当大的分歧。本研究的目的是研究存在的肽能和烟碱突触后反应在牛蛙交感神经节的突触相互作用，用细胞内和电压钳记录方法。刺激第3 ~ 5脊神经（0.2Hz）和第8脊神经（30 Hz），在同一交感神经元上均诱发快兴奋性突触后电位（EPSP）和迟发慢EPSP。在大多数神经元中，快EPSP的幅度在晚慢EPSP过程中降低。快EPSP的量子含量也减少。乙酰胆碱诱导的去极化ACh电位和电流（ACh电流）在电生理过程中没有改变或增加。 ...更多信息 迟发慢EPSP。促黄体生成素释放激素（LH-RH; 40 nM-4 M）的连续应用以浓度依赖性方式抑制快速EPSP。在浓度为1 M时，LH-RH使快EPSP的量子含量降低63.8%。LH-RH可降低微EPSP的频率。LH-RH受体拮抗剂（[D-Phe^2，6>，Pro ^3]-LH-RH和[d-pGlu^1，D-Phe^2，D-Tri^3，6> -LH-RH）可阻断LH-RH对快EPSP的突触前抑制作用。结果提示，牛蛙交感神经节突触前神经终末ACh的诱发释放减少，从而使快EPSP在慢EPSP晚期受到抑制。在某些交感神经B神经元中。LH-RH使ACh电流增加，量效曲线左移。电压钳分析表明，LH-RH不改变与烟碱受体相关的离子通道的特性。LH-TH可能通过增加ACh对受体的亲和力而促进烟碱型ACh受体的敏感性。少

Pharmacological study has reported previously modulation of cholinergic transmission induced by interaction between nicotinic and peptidergic transmitter substances. However, there was considerable disagreement among the experimental findings. The purpose of the present study was to examine the existence of synaptic interaction between peptidergic and nicotinic postsynaptic responses in bullfrog sympathetic ganglia, using intracellular and voltage-clamp recording methods. Stimulations of both 3rd-5th (0.2 Hz) and 8th (30 Hz) spinal nerves evoked the fast excitatory postsynaptic potential (EPSP) superimposed with the late slow EPSP at the same sympathetic neuron. The amplitude of the fast EPSPs was decreased during the course of the late slow EPSP in a majority of neurons. The quantal content of the fast EPSP was also decreased. Acetylcholine-induced depolarization ACh potential and current (ACh current) produced by ionophoretic application of ACh were not changed or increased during th … More e late slow EPSP. Bath-application of luteinizing hormone-releasing hormone (LH-RH; 40 nM-4 M) depressed the fast EPSP in a concentration-dependent manner. At a concentration 1 M, LH-RH produced a 63 8 % depression of the quantal content of the fast EPSP. LH-RH depressed the frequency of the miniature EPSP. Antagonists for LH-RH receptor ([D-Phe^<2,6>, Pro^3]-LH-RH and [d-pGlu^1, D-Phe^2, D-Tri^<3,6> -LH-RH) prevented the presynaptic inhibition of the fast EPSP induced by LH-RH. These results suggest that the fast EPSP is depressed during the late slow EPSP by decreasing the evoked release of ACh from presynaptic nerve terminals in bullfrog sympathetic ganglia. In some sympathetic B neurons. LH-RH increased the ACh current and shifted the dose response curve in parallel to the left. Voltage-clamp analyses using a single sympathetic neurons showed that LH-RH did not change the properties of ion channels associated with the nicotinic receptor. LH-TH may facilitate the sensitivity of the nicotinic ACh receptors by increasing an affinity of ACh to the receptor. Less