Katayama Y, Hirai K
Department of Autonomic Physiology, Medical Research Institute, Tokyo Medical and Dental University, Japan.
Brain Res. 1989 May 15;487(1):62-8. doi: 10.1016/0006-8993(89)90940-2.
Intracellular recordings were made from neurons in cat parasympathetic ciliary ganglia in vitro. Somatostatin (30 nM-3 microM) reduced the amplitude of excitatory postsynaptic potentials (EPSPs), whereas the peptide did not affect acetylcholine (ACh)-induced depolarizations. Thus somatostatin depressed the EPSPs without changing the postsynaptic sensitivity to ACh. The inhibitory action of somatostatin on the EPSPs was passed off even in the presence of the peptide at concentrations higher than 100 nM. When paired stimuli at an interval of 50 ms were applied to preganglionic nerves, the second EPSP was facilitated, being larger in amplitude than the first one; this facilitation was reversibly inhibited in the presence of the peptide. Somatostatin reversibly reduced the frequency of spontaneous EPSPs without appreciably changing their mean amplitude. All of these results indicate that somatostatin may presynaptically reduce the amount of ACh released. The mechanism underlying this action was discussed.
在体外对猫副交感神经睫状神经节中的神经元进行细胞内记录。生长抑素（30 nM - 3 μM）降低了兴奋性突触后电位（EPSP）的幅度，而该肽不影响乙酰胆碱（ACh）诱导的去极化。因此，生长抑素在不改变突触后对ACh敏感性的情况下抑制了EPSP。即使存在浓度高于100 nM的该肽，生长抑素对EPSP的抑制作用仍然存在。当以50 ms的间隔对节前神经施加成对刺激时，第二个EPSP出现易化，其幅度大于第一个；在该肽存在的情况下，这种易化被可逆性抑制。生长抑素可逆性降低了自发EPSP的频率，而未明显改变其平均幅度。所有这些结果表明，生长抑素可能在突触前减少ACh的释放量。并对该作用的潜在机制进行了讨论。
