Xi-Moy S X, Randall W C, Wurster R D
Department of Physiology, Loyola University Medical Center, Maywood, Illinois 60153.
J Auton Nerv Syst. 1993 Mar;42(3):201-13. doi: 10.1016/0165-1838(93)90365-2.
Nicotinic and muscarinic mediated synaptic mechanisms were investigated in isolated, canine intracardiac ganglia taken from the right atrial fat pad. Using conventional intracellular microelectrode recording techniques on 216 neurons, fast and slow synaptic potentials were evoked by single or trains of stimulation of presynaptic fibers in interganglionic nerves. By varying the stimulus intensity, single or multiple fast excitatory postsynaptic potentials (f-EPSPs) were evoked, indicating the convergence of synaptic inputs on these cells. These f-EPSPs often reached the action potential threshold, were enhanced by the acetylcholinesterase inhibitor physostigmine and were blocked by the nicotinic antagonist hexamethonium. The f-EPSPs were accompanied by a decreased input resistance and had an extrapolated reversal potential of -7.1 mV, suggesting increased conductances to more than one cation. Repetitive presynaptic stimulation evoked slow excitatory postsynaptic potentials (s-EPSPs) in 41% of the cells while slow inhibitory postsynaptic potentials (s-IPSPs) or s-IPSPs followed by s-EPSPs were evoked in 19% of the cells. All slow potentials were abolished by atropine and low Ca2+/high Mg2+ solutions and enhanced by physostigmine. Hexamethonium and adrenergic receptor antagonists had no effects on s-EPSP and s-IPSP. The M1 receptor antagonist pirenzepine reversibly blocked the s-EPSP but not the s-IPSP. On the other hand, the M2 receptor blocker 4-diphenyl-acetoxy-N-methyl piperidine methiodide (4-DAMP) had no effects on the s-EPSP. These observations suggest that s-EPSPs and s-EPSPs are mediated by distinct muscarinic receptors. The amplitude of the s-EPSP and the depolarization evoked by the muscarinic agonist, bethanechol were accompanied by increased input resistance. These responses were decreased in amplitude by membrane hyperpolarization and either reversed polarity or declined to zero amplitude at about -80 mV, suggesting the inhibition of a potassium conductance.
在取自右心房脂肪垫的离体犬心内神经节中，对烟碱能和毒蕈碱能介导的突触机制进行了研究。运用传统的细胞内微电极记录技术，对216个神经元进行记录，通过对神经节间神经中突触前纤维进行单次或串刺激，诱发快速和慢速突触电位。通过改变刺激强度，诱发了单个或多个快速兴奋性突触后电位（f-EPSP），表明这些细胞上存在突触输入的汇聚。这些f-EPSP常达到动作电位阈值，被乙酰胆碱酯酶抑制剂毒扁豆碱增强，并被烟碱拮抗剂六甲铵阻断。f-EPSP伴随着输入电阻降低，其外推反转电位为-7.1 mV，提示对一种以上阳离子的电导增加。重复突触前刺激在41%的细胞中诱发了慢速兴奋性突触后电位（s-EPSP），而在19%的细胞中诱发了慢速抑制性突触后电位（s-IPSP）或继之以s-EPSP的s-IPSP。所有慢速电位均被阿托品和低钙/高镁溶液消除，并被毒扁豆碱增强。六甲铵和肾上腺素能受体拮抗剂对s-EPSP和s-IPSP无影响。M1受体拮抗剂哌仑西平可逆性阻断s-EPSP，但不阻断s-IPSP。另一方面，M2受体阻滞剂4-二苯基乙酰氧基-N-甲基哌啶甲基碘化物（4-DAMP）对s-EPSP无影响。这些观察结果表明，s-EPSP和s-EPSP由不同的毒蕈碱受体介导。s-EPSP的幅度以及毒蕈碱激动剂氨甲酰甲胆碱诱发的去极化伴随着输入电阻增加。这些反应的幅度因膜超极化而降低，要么极性反转，要么在约-80 mV时幅度降至零，提示钾电导受到抑制。
