Mn and Mg influxes through Ca channels of motor nerve terminals are prevented by verapamil in frogs.
At frog neuromuscular junctions immersed in solutions containing 0.5 mM Mn2+, verapamil (40 microM) reduced the increase in miniature end-plate potential (MEPP) frequency produced by tetanic stimulation (50 Hz, 2 min) of the motor nerve to 5% of that in the absence of verapamil. In solutions containing 5 mM Mg2+, verapamil reduced the tetanic increase in MEPP frequency to 8% of that in the absence of verapamil. Verapamil added to solutions containing 0.15 mM Ca2+ decreased the tetanic rise in MEPP frequency to 6% of the control value. In low Ca2+ (nominally Ca2(+)-free) solutions, verapamil decreased the tetanic rise to 70% of the control value. The present results suggest that Mn2+ and Mg2+, as well as Ca2+, enter the nerve terminal through Ca2+ channels during nerve stimulation and promote transmitter release. In addition to its effect on the Ca2+ channel, verapamil at higher concentrations appears to have inhibitory effects on the acetylcholine-gated end-plate channel and on the Na+ channel as suggested by its depressive effects on the amplitudes of MEPPs, end-plate potentials and nerve terminal action potentials.
Narita
K
K
Department of Physiology, Kawasaki Medical School, Okayama, Japan.
Kawasaki
F
F
Kita
H
H
D000200:Action Potentials / Q000187:drug effects; D000818:Animals; D015220:Calcium Channels / Q000187:drug effects / Q000502:physiology*; D066298:In Vitro Techniques; D008274:Magnesium / Q000502:physiology*; D008345:Manganese / Q000502:physiology*; D009046:Motor Neurons / Q000187:drug effects / Q000502:physiology*; D011896:Rana temporaria / Q000502:physiology*; D014700:Verapamil / Q000494:pharmacology*
D015220:Calcium Channels; D008345:Manganese; D014700:Verapamil; D008274:Magnesium