Membrane properties and intracellular biochemical processes during vasopressin-induced bursting activity in snail neurons

• Published in: Neuroscience research Vol. 4; no. 1; p. 37
• Main Authors: Onozuka, M, Furuichi, H, Kishii, K, Imai, S
• Format: Journal Article
• Language: English
• Published: Ireland 01.11.1986
• Subjects: Adenylyl Cyclases - metabolism; Animals; Arginine Vasopressin - pharmacology; Calcium - metabolism; Cyclic AMP - metabolism; Dose-Response Relationship, Drug; Ganglia - drug effects; Ganglia - enzymology; Ion Channels - drug effects; Membrane Potentials - drug effects; Neurons - drug effects; Protein Kinases - metabolism; Snails; Synaptic Membranes - drug effects; Synaptic Transmission - drug effects
• ISSN: 0168-0102
• DOI: 10.1016/0168-0102(86)90015-5

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 Co2+-substituted Ca2+-free saline. This hormone also caused the following intracellular biochemical alterations: elevation in the cyclic AMP levels; stimulation of adenylate cyclase and Ca2+-dependent protein kinase activities; and promotion of Ca2+ release from the intracellular reservoir, lysosome-like granules. These results suggest that AVP-induced bursting activity is mediated through intracellular biochemical processes.