Morphine augments calcium-dependent potassium conductance in guinea-pig myenteric neurones.
Intracellular recordings were made from myenteric neurones removed from guinea-pig ileum and maintained in vitro. Action potentials were elicited by passing brief depolarizing currents through the recording electrode. In AH cells they were followed by afterhyperpolarizations resulting from an increase in potassium conductance (GK,Ca). Morphine (1 nM - 1 microM), applied by superfusion, increased the duration of the afterhyperpolarization (and the underlying GK,Ca) which followed from 1 to 30 action potentials. Morphine did not change the peak amplitude of the afterhyperpolarization. This action of morphine occurred both in cells which showed no change in resting membrane potential or resistance and in cells which were hyperpolarized. It was prevented by naloxone (10 nM - 1 microM). The possibility is proposed that morphine inhibits one of the mechanisms by which myenteric neurones control their free intracellular calcium concentration close to the plasma membrane.
D000200:Action Potentials / Q000187:drug effects; D000818:Animals; D002118:Calcium / Q000378:metabolism*; D004553:Electric Conductivity; D006168:Guinea Pigs; D066298:In Vitro Techniques; D008564:Membrane Potentials / Q000187:drug effects; D009020:Morphine / Q000494:pharmacology*; D009197:Myenteric Plexus / Q000502:physiology*; D009270:Naloxone / Q000494:pharmacology; D009474:Neurons / Q000378:metabolism / Q000502:physiology*; D011188:Potassium / Q000378:metabolism
D009270:Naloxone; D009020:Morphine; D011188:Potassium; D002118:Calcium