Abstract

The excitatory actions of G-protein-coupled agonists on amphibian sympathetic ganglion cells involved suppression of a voltage and time dependent, non-inactivating K +-current called the M-current. Suppression of this current by muscarine or peptides is followed by a phase of ‘over-recovery’ during which the M-current exceeds its original level. Whilst it has been suggested that release of intracellular Ca 2+ following the agonist-induced liberation of inositol 1,4,5-triphosphate is involved in the suppression phase of the response, another hypothesis suggests that the agonist-induced elevation of intracellular Ca 2+ may account for M-current ‘over-recovery’. The present study supports the latter hypothesis because intracellular application of the inositol 1,4,5-triphosphate antagonist, heparin (150 μM), had little or no effect on muscarine-induced M-current suppression whilst the ‘over-recovery’ phase of the response was markedly attenuated.

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