INVOLVEMENT OF CALCISEPTINE-SENSITIVE CALCIUM CHANNELS IN THE EVOKED ACETYLCHOLINE-RELEASE FROM ELECTRIC ORGAN SYNAPTOSOMES

Citation
H. Tokumaru et al., INVOLVEMENT OF CALCISEPTINE-SENSITIVE CALCIUM CHANNELS IN THE EVOKED ACETYLCHOLINE-RELEASE FROM ELECTRIC ORGAN SYNAPTOSOMES, Biological & pharmaceutical bulletin, 20(6), 1997, pp. 641-645
Citations number
31
Categorie Soggetti
Pharmacology & Pharmacy
ISSN journal
09186158
Volume
20
Issue
6
Year of publication
1997
Pages
641 - 645
Database
ISI
SICI code
0918-6158(1997)20:6<641:IOCCCI>2.0.ZU;2-B
Abstract
The high K+-evoked release of acetylcholine (ACh) from electric organ synaptosomes isolated from the Japanese marine ray, Narke japonica, wa s strongly inhibited by dihydropyridines at micromolar concentrations. However, this inhibition seems to be a non-specific effect since the agonist (-)-Bay K 8644 also had inhibitory effects. Calciseptine, a pe ptide toxin specific for L-type Ca channels, inhibited to a lesser ext ent the evoked acetylcholine release: the maximum inhibition was about 20%. This finding is in accord with our data (Tokumaru et al,, J, Neu rochem., 65, 831(1995)) regarding inhibition by a monoclonal antibody against the alpha(2) delta-subunit of the L-type Ca channel and provid es evidence for the involvement of an L-type-like Ca channel in ACh re lease in addition to omega-conotoxin GVIA-sensitive N-type and omega-a gatoxin IVA-sensitive P-type Ca channels.