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去甲肾上腺素和乙酰胆碱对交感神经节细胞的作用。

Actions of noradrenaline and acetylcholine on sympathetic ganglion cells.

作者信息

Kobayashi H, Libet B

出版信息

J Physiol. 1970 Jun;208(2):353-72. doi: 10.1113/jphysiol.1970.sp009125.

Abstract
  1. The responses of the post-synaptic membrane of sympathetic ganglion cells to noradrenaline (NA) and to acetylcholine (ACh) were studied in relation to the slow inhibitory post-synaptic potential (S-IPSP) and slow excitatory one (S-EPSP) respectively.2. NA produced an hyperpolarization of about 4 mV in cells of rabbit superior cervical ganglia.3. The hyperpolarizing response to NA was not accompanied by any detectable change in membrane resistance, and it was depressed by conditioning depolarization.4. NA also depressed all the post-synaptic potentials, presumably by an action on presynaptic function.5. ACh produced a large depolarization in ganglion cells of rabbit and of frog (paravertebral) ganglia, which was accompanied by a large decrease in membrane resistance.6. When ACh was applied during nicotinic blockade, achieved with high concentration of nicotine (frog ganglia) or D-tubocurarine (rabbit ganglia), it still produced a considerable depolarization. This response could be blocked by atropine, and is presumably a muscarinic type of action.7. The muscarinic-ACh response was not accompanied by a decrease in membrane resistance. Instead, the frog ganglion cells exhibited increased resistances of up to more than twice the resting value during both the muscarinic-ACh depolarization and the S-EPSP.8. The muscarinic-ACh depolarization and the S-EPSP were both depressed by conditioning hyperpolarization (in nicotinized frog cells). An initial hyperpolarizing phase now appeared in both of these responses.9. It is concluded that the hyperpolarizing response to NA and the depolarizing response to muscarinic-ACh action are not generated by increases in ionic mobilities in the post-synaptic membrane; and that these two responses are produced by the same electrogenic mechanisms which underlie the S-IPSP and the S-EPSP respectively.
摘要
  1. 研究了交感神经节细胞突触后膜对去甲肾上腺素(NA)和乙酰胆碱(ACh)的反应,分别与慢抑制性突触后电位(S-IPSP)和慢兴奋性突触后电位(S-EPSP)相关。

  2. NA使兔颈上神经节细胞产生约4 mV的超极化。

  3. 对NA的超极化反应未伴随膜电阻的任何可检测变化,且受条件性去极化抑制。

  4. NA还抑制所有突触后电位,推测是通过对突触前功能的作用。

  5. ACh使兔和蛙(椎旁)神经节细胞产生大量去极化,同时伴有膜电阻大幅降低。

  6. 当在高浓度尼古丁(蛙神经节)或筒箭毒碱(兔神经节)实现烟碱阻断期间施加ACh时,它仍产生相当大的去极化。该反应可被阿托品阻断,推测是毒蕈碱型作用。

  7. 毒蕈碱型ACh反应未伴随膜电阻降低。相反,在毒蕈碱型ACh去极化和S-EPSP期间,蛙神经节细胞的电阻增加至静息值的两倍以上。

  8. 条件性超极化(在烟碱化蛙细胞中)抑制毒蕈碱型ACh去极化和S-EPSP。现在这两种反应中均出现初始超极化阶段。

  9. 得出结论:对NA的超极化反应和对毒蕈碱型ACh作用的去极化反应不是由突触后膜离子迁移率增加产生的;并且这两种反应分别由构成S-IPSP和S-EPSP基础的相同电生机制产生。

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Responses of isolated curarized sympathetic ganglia.离体箭毒化交感神经节的反应
J Physiol. 1952 Jun;117(2):196-217. doi: 10.1113/jphysiol.1952.sp004740.
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Adrenaline and transmission in the sympathetic ganglion of the cat.肾上腺素与猫交感神经节中的神经传递
Acta Physiol Scand. 1952 Sep 10;26(2-3):252-63. doi: 10.1111/j.1748-1716.1952.tb00908.x.

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