Abstract
To elucidate the mechanism generating bursting activity, the effect of arginine vasopressin (AVP) was studied electrophysiologically and biochemically in ganglionic preparations from the snail, Euhadra peliomphala. AVP caused bursting activity which is accompanied by the development of a negative slope resistance (NSR) region in the current-voltage (I–V) curve of the identified neurons. Similar effects were observed by application of veratridine, dibutyryl cyclic AMP and isobutylmethylxanthine. Both the bursting activity and the I–V relation induced by AVP were markedly inhibited by reduction of extracellular Na + but not by Co 2+-substituted Ca 2+-free saline. This hormone also caused the following intracellular biochemical alterations: (i) elevation in the cyclic AMP levels; (ii) stimulation of adenylate cyclase and Ca 2+-dependent protein kinase activities; and (iii) promotion of Ca 2+ release from the intracellular reservoir, lysosome-like granules. These results suggest that AVP-induced bursting activity is mediated through intracellular biochemical processes.
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