Müller W E, Snyder S H
Ann Neurol. 1977 Oct;2(4):340-2. doi: 10.1002/ana.410020415.
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.
急性卟啉症的症状被认为是由δ-氨基乙酰丙酸（ALA）的作用所致。我们报告称，ALA能选择性地竞争与中枢神经系统膜中突触γ-氨基丁酸（[3H]GABA）受体相关的氚化γ-氨基丁酸的结合。抑制GABA受体结合的ALA浓度与卟啉症患者中枢神经系统中被认为存在的ALA水平一致。急性卟啉症的一些症状类似于强效GABA激动剂药物蝇蕈醇所引发的症状。加重卟啉症症状的巴比妥类药物是GABA突触作用的强效促进剂。这些结果表明，急性卟啉症的一些症状可能归因于ALA在中枢神经系统受体部位对GABA的模拟作用。
