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嗅皮质无髓鞘轴突中的突触前钠/钙动作电位。

Presynaptic Na/Ca action potentials in unmyelinated axons of olfactory cortex.

作者信息

Scholfield C N

机构信息

Department of Physiology, Queen's University, Belfast, Northern Ireland.

出版信息

Pflugers Arch. 1988 Feb;411(2):180-7. doi: 10.1007/BF00582312.

DOI:10.1007/BF00582312
PMID:3357756
Abstract

(1) Pial surface slices of guinea-pig olfactory cortex were cut to have a thickness of 150 micron. Action potentials were recorded from the sectioned ends of the unmyelinated afferent axons originating from the lateral olfactory tract (LOT). These potentials were prolonged by the K-channel blocker 3,4-diaminopyridine (0.1 mmol/l) and further lengthened by tetraethylammonium (10 mmol/l). The action potential was also greatly prolonged by partly replacing the K+ in the bathing solution by Cs+. (2) These prolonged action potentials were shortened by Cd2+; Gd3+ (gadolinium); Ni2+; Mn2+; Co2+, in order of potency. The residual early component of the action potential was tetrodotoxin (TTX) sensitive. In contrast, the LOT action potential was little affected by Ca-channel blockade. (3) Organic Ca-channel blockers either had no effect (0.05 mmol/l nifedipine), or depressed the early and later phases of the prolonged action potential equally (0.05-0.5 mmol/l verapamil or 0.05-0.2 mmol/l diltiazem). (4) A propagated action potential was also obtained in solution containing TTX and low Na+. This potential was supported by Ca2+, Sr2+ or Ba2+ and completely suppressed by Cd2+. (5) The later parts of the action potential, after K-channel blockade, had a pharmacological sensitivity towards Ca-channel blockers matching that of synaptic transmission. This suggests the falling phase of the action potential is caused by charge carrier (mainly Ca2+) passing through Ca-channels that have similar properties to, or are the same as those which open prior to transmitter release.

摘要

(1) 将豚鼠嗅皮质的软膜表面切片切成150微米厚。从源自外侧嗅束(LOT)的无髓传入轴突的切片末端记录动作电位。这些电位被钾通道阻滞剂3,4 - 二氨基吡啶(0.1 mmol/L)延长,并被四乙铵(10 mmol/L)进一步延长。通过用铯部分替代浴液中的钾离子,动作电位也大大延长。(2) 这些延长的动作电位被镉离子、钆离子、镍离子、锰离子、钴离子按效力顺序缩短。动作电位的残余早期成分对河豚毒素(TTX)敏感。相比之下,LOT动作电位受钙通道阻断的影响很小。(3) 有机钙通道阻滞剂要么没有作用(0.05 mmol/L硝苯地平),要么同等程度地抑制延长动作电位的早期和后期阶段(0.05 - 0.5 mmol/L维拉帕米或0.05 - 0.2 mmol/L地尔硫䓬)。(4) 在含有TTX和低钠的溶液中也获得了传播性动作电位。该电位由钙离子、锶离子或钡离子支持,并被镉离子完全抑制。(5) 钾通道阻断后动作电位的后期部分对钙通道阻滞剂具有与突触传递相匹配的药理学敏感性。这表明动作电位的下降阶段是由电荷载体(主要是钙离子)通过与递质释放前开放的钙通道具有相似性质或相同的钙通道引起的。

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