Inhibition of the evoked release of acetylcholine by the porphyrin precursor delta-aminolevulinic acid.
The effect of delta-aminolevulinic acid (ALA) on neuromuscular transmission were studied. High concentrations (0.6 to 18 mM) of ALA caused significant reductions in the amplitudes of curarized end-plate potentials (epps). Changing the ratio of calcium to magnesium in the bathing solution allowed the quantal content of the epps to be directly measured. Under these conditions, ALA reduced the quantal content of epps without affecting the depolarization produced by a single quantum of acetylcholine. It was concluded that ALA, in high concentrations, inhibits the release of acetylcholine evoked by a nerve impulse but is unlikely to be the cause of the neurological defects of acute porphyria.
D000109:Acetylcholine / Q000378:metabolism*; D000622:Aminolevulinic Acid / Q000494:pharmacology*; D000818:Animals; D002118:Calcium / Q000494:pharmacology; D002463:Cell Membrane Permeability / Q000187:drug effects; D066298:In Vitro Techniques; D007982:Levulinic Acids / Q000494:pharmacology*; D008274:Magnesium / Q000494:pharmacology; D008564:Membrane Potentials / Q000187:drug effects; D009469:Neuromuscular Junction / Q000187:drug effects* / Q000378:metabolism; D051381:Rats; D012964:Sodium / Q000378:metabolism; D009435:Synaptic Transmission / Q000187:drug effects
D007982:Levulinic Acids; D000622:Aminolevulinic Acid; D012964:Sodium; D008274:Magnesium; D000109:Acetylcholine; D002118:Calcium