SYNAPTIC MODULATION OF CALCIUM-DEPENDENT POTASSIUM CONDUCTANCE IN MYENTERIC NEURONS IN THE GUINEA-PIG

SYNAPTIC MODULATION OF CALCIUM-DEPENDENT POTASSIUM CONDUCTANCE IN MYENTERIC NEURONS IN THE GUINEA-PIG
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DOI:
10.1113/jphysiol.1980.sp013360
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发表时间:
1980-01-01
影响因子:
5.5
通讯作者:
WOOD, JD
WOOD, JD
中科院分区:
医学1区
文献类型:
--
作者:
GRAFE, P;MAYER, CJ;WOOD, JD

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用细胞内记录法对豚鼠小肠肌肠丛神经节细胞进行了研究。对节间连接的电刺激引起与细胞输入电阻增加相关的慢突触兴奋(慢电位)。在刺激终止后,慢速epsp持续数秒;它们只发生在动作电位之后的长时间超极化后电位的神经元中。在1-5 mM-Mn2+、16 mM-Mg2+和1 mM-Ca2+的溶液中,神经元的超融合模拟了慢速e.p.s.p.。Mn2+、Mg2+和慢速e.p.s.p.的共同特征是膜电位去极化,细胞输入电阻增加,兴奋性增强,阻断峰后超极化电位,逆转电位在-70 ~ -75 mW之间。基于常场方程的分析表明,当Ca2+内流被Mn2+或Mg2+阻断时,K+对其他渗透离子的渗透率比降低。有机钙拮抗剂D-600[甲氧基维拉帕米]对神经元无影响。肌丛兴奋性的缓慢突触调节显然涉及静息GK [K+电导]和峰后GK的减少,这是由于神经递质抑制Ca2+内流而导致的。
Ganglion cells of the myenteric plexus of the guinea-pig small intestine were studied with intracellular recording methods. Electrical stimulation of the interganglionic connectives elicted slow synaptic excitation (slow e.p.s.p.) associated with an increase in the input resistance of the cell. The slow e.p.s.p. continued for several seconds after termination of stimulation; they occurred only in neurons where prolonged hyperpolarizing after-potentials followed an action potential. Superfusion of the neurons with solutions containing 1-5 mM-Mn2+ or 16 mM-Mg2+ and 1 mM-Ca2+ mimicked the slow e.p.s.p. The common characteristics of Mn2+, Mg2+ and the slow e.p.s.p. were depolarization of the membrane potential, increased input resistance of the cell, augmented excitability, blockade of post-pike hyperpolarizing potentials and reversal potential between -70 and -75 mW. Analyses based on the constant field equation implied the permeability ratios of K+ to other permeant ionic species were reduced when Ca2+ influx was blocked by Mn2+ or Mg2+. The organic Ca antagonist D-600 [methoxy verapamil did not affect the neurons. Slow synaptic modulation of excitability within the myenteric plexus apparently involves a reduction of resting GK [conductance for K+] and post-spike GK which is secondary to suppression of Ca2+ influx by the neurotransmitter for the slow e.p.s.p.