delta-Aminolevulinic acid: influences on synaptic GABA receptor binding may explain CNS symptoms of porphyria.

Article date: 1977/10/1

PubMed ID: 214024

Journal name: Annals of neurology (ISSN: 0364-5134)


Symptoms of acute porphyria have been attributed to effects of delta-aminolevulinic acid (ALA). We report that ALA selectively competes for the binding of tritiated gamma-aminobutyric acid ([3H]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.

This document is available from: http://directlinks.cc/files/muscimol/214024.pdf

Author List: Müller W E, Snyder S H

Publication Types: Journal Article; Research Support, U.S. Gov't, P.H.S.

Substances mentioned in the article: Levulinic Acids; Receptors, Neurotransmitter; gamma-Aminobutyric Acid; Aminolevulinic Acid; Sodium; Strychnine; Glycine;

Mesh terms: Aminolevulinic Acid/blood; Animals; Anura; Binding, Competitive/drug effects; Brain/metabolism; Dose-Response Relationship, Drug; Glycine/metabolism; Levulinic Acids/pharmacology; Male; Porphyrias/blood; Rana catesbeiana; Rats; Receptors, Neurotransmitter/drug effects; Sodium/pharmacology; Spinal Cord/metabolism; Strychnine/pharmacology; Synaptosomes/metabolism; gamma-Aminobutyric Acid/metabolism;

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