Stannous chloride-induced increase in calcium entry into motor nerve terminals of the frog.
The effects of SnCl2 on potentials recorded extracellularly from motor nerve terminals of the bullfrog were studied to elucidate the mechanism of the SnCl2-induced facilitation of evoked transmitter release. Under conditions in which the muscle preparations were pretreated with d-tubocurarine and tetraethylammonium in a K+-free medium, SnCl2 (50 microM) augmented the prolonged positive deflection ascribed to the inward Ca2+ current, an effect which was reduced by addition of Cd2+. The results suggest that SnCl2 could increase Ca2+ entry into the nerve terminals.
Hattori
T
T
Department of Dental Pharmacology, Matsumoto Dental College, Shiojiri, Japan.
Maehashi
H
H
D000200:Action Potentials / Q000187:drug effects; D000818:Animals; D002118:Calcium / Q000378:metabolism*; D066298:In Vitro Techniques; D009046:Motor Neurons / Q000187:drug effects / Q000378:metabolism*; D018377:Neurotransmitter Agents / Q000378:metabolism; D015221:Potassium Channels / Q000187:drug effects; D011892:Rana catesbeiana; D014001:Tin / Q000494:pharmacology*; D017971:Tin Compounds; D014403:Tubocurarine / Q000494:pharmacology
D018377:Neurotransmitter Agents; D015221:Potassium Channels; D017971:Tin Compounds; C023599:stannous chloride; D014001:Tin; D002118:Calcium; D014403:Tubocurarine