Somatostatin presynaptically inhibits transmitter release in feline parasympathetic ganglia.
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.
Katayama
Y
Y
Department of Autonomic Physiology, Medical Research Institute, Tokyo Medical and Dental University, Japan.
Hirai
K
K
D000109:Acetylcholine / Q000378:metabolism*; D000200:Action Potentials / Q000187:drug effects; D000818:Animals; D002415:Cats; D005260:Female; D005726:Ganglia, Parasympathetic / Q000187:drug effects / Q000378:metabolism*; D008297:Male; D013004:Somatostatin / Q000494:pharmacology*; D009435:Synaptic Transmission / Q000187:drug effects
D013004:Somatostatin; D000109:Acetylcholine