Konopka L M, Parsons R L
Department of Anatomy and Neurobiology, College of Medicine, University of Vermont, Burlington 05405.
Neurosci Lett. 1989 Apr 24;99(1-2):142-6. doi: 10.1016/0304-3940(89)90279-6.
The depolarization of mudpuppy parasympathetic cardiac neurons, produced by pressure application of the neuropeptide galanin, has been characterized. The amplitude and duration of the depolarization were dependent on the duration of the galanin application. The amplitude of the depolarization increased with hyperpolarization and the reversal potential determined by extrapolation was approximately +10 mV. The amplitude and time course of the galanin-induced depolarization were not changed by substitution of either manganese or magnesium for extracellular calcium, but were decreased by exposure to 50-100 microM d-tubocurarine. It is proposed that the galanin-induced depolarization results from a receptor-activated, nonselective, cation channel; and further, that the receptor initiating depolarization differs from the galanin receptor mediating hyperpolarizing responses in these parasympathetic neurons.
通过施加神经肽甘丙肽产生的泥螈副交感神经心脏神经元的去极化已得到表征。去极化的幅度和持续时间取决于甘丙肽施加的持续时间。去极化的幅度随超极化而增加，通过外推法确定的反转电位约为 +10 mV。用锰或镁替代细胞外钙不会改变甘丙肽诱导的去极化的幅度和时间进程，但暴露于50 - 100 microM的d - 筒箭毒碱会使其降低。有人提出，甘丙肽诱导的去极化是由受体激活的、非选择性阳离子通道引起的；此外，引发去极化的受体与介导这些副交感神经元超极化反应的甘丙肽受体不同。
