Smith P A, Weight F F
J Neurophysiol. 1986 Sep;56(3):823-34. doi: 10.1152/jn.1986.56.3.823.
Intracellular and sucrose gap recording techniques were used to examine synaptically evoked potentials and the response of neurons in bullfrog paravertebral sympathetic ganglia to muscarinic agonists. These neurons were defined as either B or C cells on the basis of the conduction velocity of antidromically evoked action potentials. Following stimulation of preganglionic C-fibers in the rostral portion of the VIIIth spinal nerve, a fast nicotinic excitatory postsynaptic potential (EPSP) and a slow atropine-sensitive inhibitory postsynaptic potential (IPSP) could be recorded intracellularly in C cells of the IXth and Xth paravertebral ganglia treated with 70 microM d-tubocurarine chloride (dTC). Under these conditions, local iontophoretic application of acetylcholine (ACh) could produce a slow hyperpolarization of C cell membrane potential. ACh hyperpolarizations or slow IPSPs were not detected in ganglionic B cells. Stimulation of the preganglionic B-fibers in the sympathetic chain produced a fast nicotinic EPSP and a slow muscarinic EPSP in ganglionic B cells. A small population of C cells also received cholinergic B-fiber innervation from the sympathetic chain and exhibited a slow IPSP upon tetanic stimulation of this pathway. When curarized ganglia were examined by means of sucrose gap recording, superfusion of the muscarinic agonist, methacholine (MCh), produced an initial hyperpolarization (MChH) followed by a depolarization (MChD). Both responses were blocked by atropine and therefore presumably reflect the activation of muscarinic receptors involved in the generation of the slow IPSP and the slow EPSP, respectively. Although synaptic transmission was blocked by Ringer solution containing 4 mM Co2+, neither this solution nor 10 microM tetrodotoxin reduced the amplitude of the MChH. The MChH was slightly reduced by Ringer solution containing 0.1 mM Ca2+, however, the response could be restored by the addition of 6 mM Mg2+. These results indicate that the MChH in curarized bullfrog sympathetic ganglia results from a direct muscarinic action on ganglionic cells. This suggests that the slow IPSP is mediated by ACh released from cholinergic preganglionic fibers that make synaptic contact with ganglionic C cells.
采用细胞内记录和蔗糖间隙记录技术，研究牛蛙椎旁交感神经节中突触诱发电位以及神经元对毒蕈碱受体激动剂的反应。根据逆向诱发动作电位的传导速度，将这些神经元定义为B细胞或C细胞。在第VIII对脊神经头端部分的节前C纤维受到刺激后，在用70微摩尔氯化筒箭毒碱（dTC）处理的第IX和第X椎旁神经节的C细胞内，可记录到快速烟碱型兴奋性突触后电位（EPSP）和缓慢的阿托品敏感型抑制性突触后电位（IPSP）。在这些条件下，局部离子电泳施加乙酰胆碱（ACh）可使C细胞膜电位产生缓慢的超极化。在神经节B细胞中未检测到ACh超极化或缓慢的IPSP。刺激交感链中的节前B纤维，可在神经节B细胞中产生快速烟碱型EPSP和缓慢毒蕈碱型EPSP。一小部分C细胞也接受来自交感链的胆碱能B纤维支配，在强直刺激该通路时表现出缓慢的IPSP。当用蔗糖间隙记录法检查经箭毒处理的神经节时，毒蕈碱受体激动剂乙酰甲胆碱（MCh）灌流可产生初始超极化（MChH），随后是去极化（MChD）。两种反应均被阿托品阻断，因此推测分别反映了参与缓慢IPSP和缓慢EPSP产生的毒蕈碱受体的激活。尽管含有4毫摩尔Co2+的林格氏液可阻断突触传递，但该溶液和10微摩尔河豚毒素均未降低MChH的幅度。含有0.1毫摩尔Ca2+的林格氏液可使MChH略有降低，然而，加入6毫摩尔Mg2+可使反应恢复。这些结果表明，经箭毒处理的牛蛙交感神经节中的MChH是毒蕈碱对神经节细胞的直接作用所致。这表明缓慢的IPSP是由与神经节C细胞形成突触联系的胆碱能节前纤维释放的ACh介导的。
