Electronic properties of motor nerve terminals.
To obtain information about the electric membrane properties of frog motor nerve terminals we examined how depolarizing or hyperpolarizing current pulses of 2-8 ms duration to the preterminal, by electrotonic spread of potential, affected depolarization induced transmitter release. Sodium channels were blocked by tetrodotoxin. Under this condition a hyperpolarizing current pulse produced inhibition of release, followed by potentiation of release. Inhibition lasted more than 100 ms with a time constant of 50-150 ms. When, in addition, potassium channels were blocked by 3,4-diaminopyridine or tetraethylammonium a depolarizing current pulse potentiated transmitter release for a period up to 50 ms. The results imply that inward currents in the nerve terminal are carried mainly by sodium and calcium ions and outward currents by potassium ions while "leak" conductances are negligible. A low "leak" conductance and therefore a high specific membrane resistance facilitates the spread of electronic potentials and thereby explains the longlasting effects on transmitter release of brief current pulses to the preterminal.
D015761:4-Aminopyridine / Q000031:analogs & derivatives*; D000077770:Amifampridine; D000631:Aminopyridines / Q000494:pharmacology; D000818:Animals; D005071:Evoked Potentials / Q000187:drug effects; D008564:Membrane Potentials / Q000187:drug effects; D009045:Motor Endplate / Q000502:physiology*; D009046:Motor Neurons / Q000502:physiology*; D009469:Neuromuscular Junction / Q000502:physiology*; D011896:Rana temporaria; D009435:Synaptic Transmission / Q000187:drug effects; D013757:Tetraethylammonium Compounds / Q000494:pharmacology; D013779:Tetrodotoxin / Q000494:pharmacology
D000631:Aminopyridines; D013757:Tetraethylammonium Compounds; D013779:Tetrodotoxin; D015761:4-Aminopyridine; D000077770:Amifampridine