Electrotonic depolarization of nerve terminals causes a normorphine-resistant release of transmitter.
In the presence of tetrodotoxin (0.5 microM) electrical stimuli of high current strength and long impulse duration evoke the outflow of previously incorporated 3H-noradrenaline from the mouse vas deferens. The mechanism of action is probably an electrotonic depolarization of nerve terminals. The effect of normorphine, calcium and magnesium was compared on transmitter outflow evoked by conducted action potentials and electrotonic depolarization of nerve terminals. It is suggested that in the presence of tetrodotoxin electrical stimulation induces an asynchronous quantal release of transmitter.
D000200:Action Potentials / Q000187:drug effects; D000818:Animals; D002118:Calcium / Q000494:pharmacology; D004558:Electric Stimulation; D008274:Magnesium / Q000494:pharmacology; D008297:Male; D051379:Mice; D008815:Mice, Inbred Strains; D009022:Morphine Derivatives / Q000494:pharmacology*; D009474:Neurons / Q000187:drug effects / Q000502:physiology; D013779:Tetrodotoxin / Q000494:pharmacology; D014649:Vas Deferens / Q000187:drug effects / Q000294:innervation* / Q000502:physiology
D009022:Morphine Derivatives; D013779:Tetrodotoxin; D008274:Magnesium; D002118:Calcium; C010616:normorphine