Intracellular study of tonic-type enteric neurons in guinea pig small intestine.
Intracellular study of tonic-type enteric neurons in guinea pig small intestine.
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豚鼠小肠强直型肠神经元的细胞内研究。
DOI：
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发表时间：
1979
期刊：
影响因子：
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通讯作者：
Mayer Cj
中科院分区：
文献类型：
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作者：
Wood Jd;Mayer Cj
1. 细胞内记录显示，肌肠神经元群具有电行为，似乎与早期研究中利用单个单位的细胞外记录发现的强直型机械敏感神经元相当。2. 节间纤维束的电刺激在这些细胞中引起了一个缓慢上升的兴奋性突触后电位（慢EPSP），在刺激终止后延长了几秒钟。慢速EPSP与输入阻力增加和体膜兴奋性增强有关。在没有纤维束刺激的情况下，体膜的兴奋性相对较低。这表明：1)去极化电流脉冲不能引起某些细胞的尖峰放电；(2)当去极化电流脉冲引起尖峰时，只在脉冲开始时出现1 ~ 3个尖峰；3)细胞突峰电流对体细胞的被动侵入不触发突峰；4)尖峰之后是与输入电阻降低相关的超极化后电位延长。3. 慢速EPSP过程中兴奋性增强的特征有：1)内源性脉冲放电，2)持续200 ms的去极化电流脉冲放电，3)触发小体峰过程产生的电紧张性峰电位，4)超极化后峰后电位减少或消除。4. 在含有16 mM Mg+2的Krebs溶液和含有1 mM Mn2+的hepes缓冲Krebs中，慢速EPSP被还原或消除。在3倍于正常Ca2+的Krebs溶液中增强。Ca2+升高的尖峰放电消除了与慢速EPSP相关的输入电阻的增加。5. 钙的可用性是调节核周膜电导和兴奋性的重要因素。慢速EPSP提供了一种机制，即多极神经元的胞体在其树突和轴突之间抑制兴奋的传播。
1. Intracellular recording revealed a population of myenteric neurons with electrical behavior that appeared to be equivalent to the tonic-type mechanosensitive neurons found in earlier studies that utilized extracellular recording of single units. 2. Electrical stimulation of the interganglionic fiber tracts evoked a slowly rising excitatory postsynaptic potential (slow EPSP) that was prolonged for several seconds after termination of the stimulus in these cells. The slow EPSP was associated with increased input resistance and augmented excitability of the somal membrane. The somal membranes had relatively low excitability in the absence of fiber tract stimulation. This was indicated by: 1) failure of depolarizing current pulses to elicit spike discharge in some cells; 2) when spikes were elicited by depolarizing current pulses, one to three spikes occurred, and these were seen only at the onset of the pulse; 3) passive invasion of the soma by current from spikes in the cell's processes did not trigger spikes; 4) the spikes were followed by prolonged hyperpolarizing afterpotentials associated with decreased input resistance. 3. Characteristics of the augmented excitability during the slow EPSP were: 1) endogenous discharge of trains of spikes, 2) spike discharge throughout 200 ms duration depolarizing current pulses, 3) electrotonic spike potentials from the processes triggered somal spikes, 4) postspike afterhyperpolarization was reduced or abolished. 4. The slow EPSP was reduced or abolished in Krebs solution with 16 mM Mg+2 and in HEPES-buffered Krebs with 1 mM Mn2+. It was enhanced in Krebs solution with 3 times normal Ca2+. Spike discharge in elevated Ca2+ eliminated the increase in input resistance associated with the slow EPSP. 5. Calcium availability was an important factor in regulation of membrane conductance and excitability in the perikaryon. The slow EPSP provides a mechanism whereby the soma of a multipolar neuron gates the spread of excitation between its dendrites and axon.