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δ‐Aminolevulinic acid: Influences on synaptic GABA receptor binding may explain CNS symptoms of porphyria
Author(s) -
Müller Walter E.,
Snyder Solomon H.
Publication year - 1977
Publication title -
annals of neurology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 4.764
H-Index - 296
eISSN - 1531-8249
pISSN - 0364-5134
DOI - 10.1002/ana.410020415
Subject(s) - porphyria , muscimol , central nervous system , gabaa receptor , agonist , receptor , medicine , acute intermittent porphyria , gamma aminobutyric acid , endocrinology , gaba receptor , chemistry , pharmacology , neuroscience , biology
Symptoms of acute porphyria have been attributed to effects of δ‐aminolevulinic acid (ALA). We report that ALA selectively competes for the binding of tritiated γ‐aminobutyric acid ([ 3 H]GABA) associated with synaptic GABA receptors in central nervous system membranes. Concentrations of ALA that inhibit GABA receptor binding are consistent with levels of ALA thought to exist in the central nervous system of porphyric patients. Some of the symptoms of acute porphyria resemble those elicited by muscimol, a potent GABA agonist drug. Barbiturates, which exacerbate porphyric symptoms, are potent facilitators of the synaptic actions of GABA. The results suggest that some symptoms of acute porphyria might be attributable to a mimicking by ALA of GABA at its central nervous system receptor sites.