Abstract
2-Phenylethylamine (PEA) is an endogenous brain amine which probably modulates affective behavior. Using a gas-liquid chromatographic method for the quantification of PEA (as its dinitrophenyl-sulfonic acid derivative), we found in rabbits 340.9 ± 45.8 ng of PEA/g of wet brain. Brain PEA levels were markedly decreased by the ip administration of 200 mg/Kg, 4 hrs before sacrifice, of the L-aromatic amino acid decarboxylase inhibitors α-methyldopa (28.2 ± 5.1 ng/g), L-α-methyldopa hydrazine (MK-486 [66.9 ± 13.0 ng/g]) or a combination of both (30.0 ± 3.3 ng/g). Since MK-486 inhibits only peripheral decarboxylase, brain PEA must be in part of peripheral origin. Another decarboxylase inhibitor, RO 4-4602 mg/Kg, 4 hrs before sacrifice) failed to affect brain PEA content. D-amphetamine (10 mg/Kg) induced a small depletion of PEA after 30 min in untreated animals; when given in combination with RO 4-4602, brain PEA content was markedly decreased. This supports the view that amphetamine releases PEA and stimulates its synthesis.
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