Molgó J, Lemeignan M, Lechat P
Eur J Pharmacol. 1979 Jan 15;53(3):307-11. doi: 10.1016/0014-2999(79)90138-9.
4-Aminopyridine (4-AP) increased the quantal content (m) of end-plate potentials (e.p.p.s) evoked by continual stimulation (0.2--25 Hz) in frog end-plates depressed by Mg2+. The increase in m was due to an increase in the binomial parameter n. This was interpreted to mean that 4-AP increased the number of activated release sites. In junctions blocked by d-tubocurarine, 4-AP first increased and then decreased the amplitude of e.p.p.s. elicited during a train of stimuli of increasing frequency, indicating that 4-AP increased transmitter release more than mobilization.
4-氨基吡啶(4-AP)可增加被Mg2+抑制的蛙终板在持续刺激(0.2 - 25Hz)时诱发的终板电位(e.p.p.s)的量子含量(m)。m的增加是由于二项式参数n的增加。这被解释为意味着4-AP增加了活化释放位点的数量。在被d-筒箭毒碱阻断的接头中,4-AP在一系列频率递增的刺激过程中,首先增加然后降低e.p.p.s的幅度,表明4-AP增加递质释放的作用大于其动员作用。