Does phenylethylamine act as an
endogenous amphetamine in some patients?
by
Janssen PA, Leysen JE, Megens AA, Awouters FH.
Centre for Molecular Design,
Janssen Research Foundation,
B-2340 Beerse, Belgium.
Int J Neuropsychopharmcol 1999 Sep; 2(3):229-240

ABSTRACT

In brain capillary endothelium and catecholaminergic terminals a single decarboxylation step effected by aromatic amino-acid decarboxylase converts phenylalanine to phenylethylamine, at a rate comparable to that of the central synthesis of dopamine. Phenylethylamine, however, is not stored in intra-neuronal vesicles and is rapidly degraded by monoamine oxidase-B. Despite its short half-life, phenylethylamine attracts attention as an endogenous amphetamine since it can potentiate catecholaminergic neurotransmission and induce striatal hyperreactivity. Subnormal phenylethylamine levels have been linked to disorders such as attention deficit and depression; the use of selegiline (Deprenyl) in Parkinson's disease may conceivably favour recovery from deficient dopaminergic neurotransmission by a monoamine oxidase-B inhibitory action that increases central phenylethylamine. Excess phenylethylamine has been invoked particularly in paranoid schizophrenia, in which it is thought to act as an endogenous amphetamine and, therefore, would be antagonized by neuroleptics. The importance of phenylethylamine in mental disorders is far from fully elucidated but the evolution of phenylethylamine concentrations in relation to symptoms remains a worthwhile investigation for individual psychotic patients.

PEA
Caries
Magnesium
Headaches?
Consumption
Theobromine
The Chocuhaler
PEA and exercise
Food of the gods?
Phenylethylamine
Chocolate hotlinks
Chocolate: history
PEA (from PiHKAL)
PEA and dopamine
Stoned chocaholics?
PEA and antidepressants
Chocolate: food or drug?
PEA and antidepressants
Doped horses/chocolate-coated peanuts


HOME