Somatostatin Release from Rat Cerebral Cortex Synaptosomes

Publisher Website
Google Scholar
Abstract
Rat cerebral cortex synaptosomes were exposed in superfusion to various depolarizing stimuli and the release of somatostatin‐like immunoreactivity (SRIF‐LI) was measured by means of a radioimmunoassay procedure. High KC1 (9‐50 mM) concentration dependently evoked SRIF‐LI release; the evoked overflow reached a plateau at 25 mM KC1 and was completely abolished when Ca2+ ions were omitted from the superfusion medium, independently of the concentration of KC1 used. The 15 mM K+‐evoked release of SRIF‐ LI increased sharply as the Ca2+ concentration was raised to 0.8 mM, then leveled off and reached a plateau at 1.2 mM. The 15 mM K+‐evoked overflow, but not the spontaneous outflow, was partially decreased (50%) by 1 μM tetrodotoxin. The presence in the superfusion fluid of a mixture of peptidase inhibitors did not improve the recovery of SRIF‐LI both in the absence and in the presence of high K+. Exposure of synaptosomes to veratrine (1‐50 μM) induced release of SRIF‐LI in a concentration‐dependent way. The effect of the alkaloid was strictly Ca2+ and tetrodotoxin sensitive. Replacement of extracellular Na+ by sucrose caused an acceleration of the spontaneous SRIF‐LI outflow that was inversely correlated to the Na+ content in the superfusion medium. The release evoked by the sodium‐deprived media did not exhibit any calcium dependence. HPLC analysis of the samples collected during superfusion showed that >90% of the SRIF‐LI released either during the spontaneous outflow or by 15 mM KC1 was represented by SRIF‐14 (SRIF‐2814‐28). These values reflected the ratio SRIF‐14/SRIF‐28 found in synaptosomes at the end of the experiments.