Wouters W, Van Den Bercken J
Eur J Pharmacol. 1979 Aug 15;57(4):353-63. doi: 10.1016/0014-2999(79)90498-9.
The influence of ACTH4-10, a behaviourally active fragment of adrenocorticotropic hormone (ACTH) devoid of endocrine activity, on synaptic transmission in the paravertebral sympathetic ganglion of the frog was investigated. Postsynaptic potentials evoked by electrical stimulation of pregnanglionic nerves were recorded using a sucrose gap method. Fast excitatory postsynaptic potentials (EPSPs), which are mediated via nicotinic cholinergic synapses, were not affected by 10(-6) M ACTH4-10. Application of ACTH4-10 in a concentration as low as 10(-8) M for 60 min caused a marked augmentation of the amplitude of slow inhibitory postsynaptic potentials (IPSPs) which are mediated via dopaminergic synapses. The increase in amplitude developed gradually after a latency of 60--90 min and outlasted the application of the peptide. In addition, ACTH4-10 at 10(-6) M increased the hyperpolarising response of the ganglion to exogenous dopamine, as studied by a micro-application method. There was no significant effect of ACTH4-10 on the muscarinic cholinergic depolarising response of the ganglion towards exogenous acetylcholine. The behaviourally active vasopressin fragment DG-LVP (10(-6) M) had no effect on slow IPSPs. The results demonstrate that ACTH4-10 specifically affects slow synaptic inhibition in frog sympathetic ganglion, probably by acting upon the postsynaptic membrane. The possibility is discussed that ACTH4-10 affects one of the intermediate steps between dopaminergic receptor interaction and generation of the slow IPSP.
研究了促肾上腺皮质激素（ACTH）的行为活性片段ACTH4 - 10（无内分泌活性）对青蛙椎旁交感神经节突触传递的影响。采用蔗糖间隙法记录节前神经电刺激诱发的突触后电位。通过烟碱型胆碱能突触介导的快速兴奋性突触后电位（EPSP）不受10⁻⁶ M ACTH4 - 10的影响。以低至10⁻⁸ M的浓度应用ACTH4 - 10 60分钟，可使通过多巴胺能突触介导的慢抑制性突触后电位（IPSP）的幅度显著增大。幅度增加在60 - 90分钟的潜伏期后逐渐出现，并在肽的应用结束后仍持续存在。此外，通过微量应用法研究发现，10⁻⁶ M的ACTH4 - 10增加了神经节对外源性多巴胺的超极化反应。ACTH4 - 10对神经节对外源性乙酰胆碱的毒蕈碱型胆碱能去极化反应没有显著影响。具有行为活性的血管加压素片段DG - LVP（10⁻⁶ M）对慢IPSP没有影响。结果表明，ACTH4 - 10可能通过作用于突触后膜，特异性地影响青蛙交感神经节中的慢突触抑制。文中讨论了ACTH4 - 10影响多巴胺能受体相互作用与慢IPSP产生之间中间步骤之一的可能性。
