Functional interconnection between cholinergic and peptidergic neurons in bullfrog sympathetic ganglia

药理学研究先前已经报道了由烟碱和多肽递质之间的相互作用诱导的胆碱能传递的调节。然而，在实验结果中存在相当大的分歧。本研究旨在探讨牛蛙交感神经节中肽能和尼古丁突触后反应之间是否存在突触相互作用，采用细胞内和电压钳记录方法。刺激第3 -5脊神经（0.2 Hz）和第8脊神经（30 Hz）在同一交感神经元上均可诱发快速兴奋性突触后电位（EPSP）和晚慢速EPSP叠加。大多数神经元在后期慢速EPSP过程中，快速EPSP的振幅有所下降。快速EPSP的量子含量也有所降低。乙酰胆碱诱导的去极化乙酰胆碱电位和乙酰胆碱离子电泳产生的乙酰胆碱电流（ACh电流）在EPSP过程中没有改变或增加。促黄体生成素释放激素（LH-RH; 40 nM-4 M）浴用后EPSP呈浓度依赖性降低。在浓度为1 M时，LH-RH可使快速EPSP的量含量降低63.8%。LH-RH降低了微型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）阻止了LH-RH诱导的快速EPSP的突触前抑制。上述结果表明，快速EPSP在慢速EPSP后期受到抑制，其机制是通过减少牛蛙交感神经节突触前神经末梢乙酰胆碱的释放。在一些交感B神经元中。LH-RH使乙酰胆碱电流增大，剂量响应曲线平行左移。使用单个交感神经元的电压钳分析表明，rh - rh不改变与烟碱受体相关的离子通道的性质。LH-TH可能通过增加乙酰胆碱对受体的亲和力来促进烟碱乙酰胆碱受体的敏感性。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