Facilitatory effects of 4-aminopyridine on strontium-mediated evoked and delayed transmitter release from motor nerve terminals.
The effect of 4-aminopyridine (4-AP) on Sr-mediated evoked and delayed transmitter release at the frog neuromuscular junction was examined using conventional electrophysiological techniques. 4-AP (5-50 microM) increased transmitter release evoked in response to conducted nerve impulses or to electrotonic depolarization of tetrodotoxin (TTX)-treated motor nerve terminals. Spontaneous quantal transmitter release was not affected by the drug as judged by the lack of effect on miniature end-plate potentials (MEPPs) frequency. However, 4-AP (10-20 microM) markedly enhanced the frequency of MEPPs appearing during conducted low rate repetitive nerve impulses or single electrotonic depolarization of TTX-blocked nerve terminals. The results suggest that 4-AP increases the influx of Sr2+ into nerve terminals in a way that modifies its sequestration and removal by the subcellular elements of the terminal.
D015761:4-Aminopyridine; D000631:Aminopyridines / Q000494:pharmacology*; D000818:Animals; D001001:Anura; D004558:Electric Stimulation; D066298:In Vitro Techniques; D009046:Motor Neurons / Q000187:drug effects / Q000378:metabolism*; D009411:Nerve Endings / Q000187:drug effects / Q000378:metabolism*; D018377:Neurotransmitter Agents / Q000378:metabolism*; D011893:Rana esculenta; D013324:Strontium / Q000494:pharmacology*; D013779:Tetrodotoxin / Q000494:pharmacology
D000631:Aminopyridines; D018377:Neurotransmitter Agents; D013779:Tetrodotoxin; D015761:4-Aminopyridine; D013324:Strontium