δ‐Aminolevulinic acid: Influences on synaptic GABA receptor binding may explain CNS symptoms of porphyria

Walter E. Müller, Solomon H. Snyder

Research output: Contribution to journalArticlepeer-review

Abstract

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 ([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.

Original languageEnglish (US)
Pages (from-to)340-342
Number of pages3
JournalAnnals of neurology
Volume2
Issue number4
DOIs
StatePublished - Oct 1977

ASJC Scopus subject areas

  • Neurology
  • Clinical Neurology

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