The role of endogenously released arachidonic acid in the control of the NMDA (50 microM)-evoked release of [3H]-acetylcholine previously formed from [3H]-choline was investigated in striosome-enriched areas and in the matrix of the rat striatum using a microsuperfusion procedure in vitro. Experimen
Inhibition of the evoked release of acetylcholine by the porphyrin precursor δ-aminolevulinic acid
✍ Scribed by Joel C. Bornstein; Jackson B. Pickett; Dr Ivan Diamond
- Publisher
- John Wiley and Sons
- Year
- 1979
- Tongue
- English
- Weight
- 284 KB
- Volume
- 5
- Category
- Article
- ISSN
- 0364-5134
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✦ Synopsis
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.
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