Proctolin activates a slow, voltage-dependent sodium current in motoneurons of the lobster cardiac ganglion.
The two-electrode voltage-clamp technique was used to study the ionic basis of the slow depolarization caused by the neuropeptide proctolin. At negative membrane potentials, proctolin caused a dose-dependent slow inward current. This current reversed and became outward at membrane potentials positive to 0 to +20 mV. Current-voltage curves also showed the response to be voltage-dependent, with a reversal potential at positive membrane potentials. The response was blocked in sodium-free solutions. Solutions with reduced sodium concentration caused a shift of the reversal potential in a manner expected for a response that is largely sodium-dependent. We conclude that proctolin causes an inward current by increasing a voltage-dependent cation conductance that is predominantly permeable to sodium.
Freschi
J E
JE
Department of Neurology, School of Medicine, Emory University, Atlanta, GA 30322.
D000818:Animals; D005724:Ganglia / Q000187:drug effects / Q000502:physiology*; D066298:In Vitro Techniques; D008564:Membrane Potentials / Q000187:drug effects; D009046:Motor Neurons / Q000187:drug effects / Q000502:physiology*; D008121:Nephropidae / Q000502:physiology*; D009479:Neuropeptides; D009842:Oligopeptides / Q000494:pharmacology*; D012964:Sodium / Q000502:physiology*
D009479:Neuropeptides; D009842:Oligopeptides; C011536:proctolin; D012964:Sodium