Cation dependence of posttetanic potentiation of neuromuscular transmission.
We have investigated the possibility that much of posttetanic potentiation (PTP) of quantal release of neurotransmitter at the frog neuromuscular junction may be due to posttetanic accumulation of [Ca2+]i, via a plasmalemmal Cao2+-Nai+ exchanger that is powered by an increase in Nai+ during the tetanus. Our new findings on the cationic dependence of PTP are consistent with this hypothesis. 1) Several manuevers that decrease Na+-K+ pump activity, (decreasing [K+]o, replacing K+o with Rb+o or Li+o, or adding acetylstrophanthidin to Ringers), all increase the intratetanic rise and prolong the posttetanic decay of epp quantal content (m) and miniature epp frequency (fmepp). 2) Increasing [Ca2+]i or [Sr2+]o, but not [Mg2+]o, increases posttetanic fmepp in a graded fashion. 3) PTP of fmepp is still present after addition of Mn2+o, which blocks voltage dependent Ca2+ entry.
D000818:Animals; D002118:Calcium / Q000494:pharmacology*; D002412:Cations; D066298:In Vitro Techniques; D007700:Kinetics; D008094:Lithium / Q000494:pharmacology; D008274:Magnesium / Q000494:pharmacology; D009119:Muscle Contraction / Q000187:drug effects; D009469:Neuromuscular Junction / Q000187:drug effects / Q000502:physiology*; D011188:Potassium / Q000494:pharmacology*; D011894:Rana pipiens; D012413:Rubidium / Q000494:pharmacology; D013324:Strontium / Q000494:pharmacology
D002412:Cations; D008094:Lithium; D008274:Magnesium; D012413:Rubidium; D011188:Potassium; D002118:Calcium; D013324:Strontium