Heparin prevents M-current over-recovery but not M-current suppression in bullfrog sympathetic ganglion neurones.
The excitatory actions of G-protein-coupled agonists on amphibian sympathetic ganglion cells involve 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 Ca2+ following the agonist-induced liberation of inositol 1,4,5-trisphosphate is involved in the suppression phase of the response, another hypothesis suggests that the agonist-induced elevation of intracellular Ca2+ may account for M-current 'over-recovery'. The present study supports the latter hypothesis because intracellular application of the inositol 1,4,5-trisphosphate antagonist, heparin (150 microM), had little or no effect on muscarine-induced M-current suppression whilst the 'over-recovery' phase of the response was markedly attenuated.
Chen
H
H
Department of Pharmacology, University of Alberta, Edmonton, Canada.
Kurenny
D E
DE
Smith
P A
PA
D000818:Animals; D002118:Calcium / Q000378:metabolism*; D005728:Ganglia, Sympathetic / Q000166:cytology / Q000187:drug effects*; D006493:Heparin / Q000494:pharmacology*; D015544:Inositol 1,4,5-Trisphosphate / Q000378:metabolism; D009116:Muscarine / Q000494:pharmacology*; D009474:Neurons / Q000187:drug effects*; D015221:Potassium Channels / Q000187:drug effects*; D011892:Rana catesbeiana
D015221:Potassium Channels; D009116:Muscarine; D015544:Inositol 1,4,5-Trisphosphate; D006493:Heparin; D002118:Calcium