Investigations on the mechanism of cyclic guanosine monophosphate increase due to depolarizing agents as studied with sea anemone toxin II in mouse cerebellar slices

Publisher Website
Google Scholar
Abstract
Sea anemone toxin II (ATX II) and MCD-peptide, like other depolarizing agents, raise the content of cGMP and to a lesser extent of cAMP in mouse cerebellar slices. Na+ influx and Ca2+ movement are involved in their mode of action, as indicated by the following observations: The rise of cGMP due to ATX II, MCD-peptide and high potassium was diminished when Na+ had been replaced by Li+. The effects of both toxins and veratridine, but not of high potassium stimulation were prevented by tetrodotoxin (TTX). The cGMP accumulation due to both toxins was abolished in the absence of extracellular Ca2+. The so-called Ca2+-antagonist (−)-D-600 blocked the increase of cGMP due to ATX II, MCD-peptide, veratridine and high potassium. ATX II stimulated the 45Ca2+ uptake in mouse cerebellar slices which was prevented by TTX and (−)-D-600.

This publication has 37 references indexed in Scilit: