A behavioural and pharmacological examination of phenylethylamine-induced anorexia and hyperactivity--comparisons with amphetamine.
The discovery that trace amine beta-phenylethylamine (PEA) has a number of properties in common with amphetamine (AMPH) has led to the suggestion that PEA may be a neuromodulator of catecholamine release or an "endogenous amphetamine." The present study compared PEA-induced behavioural changes (anorexia and hyperactivity) with AMPH-induced changes in feeding and motor activity. The first experiment examined the effects of PEA (0-35 mg/kg) on the temporal profile of feeding. The results from this experiment revealed important differences between the effects of PEA as compared with AMPH, in particular PEA failed to increase the rate of eating that is characteristic of AMPH-induced anorexia. The second experiment concurrently measured food intake and motor activity following equi-anorectic doses of PEA and AMPH and pretreatment with the neuroleptic pimozide. Pimozide attenuated PEA-induced hyperactivity, AMPH-induced hyperactivity and AMPH-induced anorexia, but failed to attenuate PEA-induced anorexia. These findings are discussed in relation to the possible mechanisms of action of PEA and AMPH.
D000818:Animals; D003913:Dextroamphetamine / Q000494:pharmacology*; D005247:Feeding Behavior / Q000187:drug effects*; D008297:Male; D009043:Motor Activity / Q000187:drug effects*; D010627:Phenethylamines / Q000494:pharmacology*; D010868:Pimozide / Q000494:pharmacology; D051381:Rats
D010627:Phenethylamines; D010868:Pimozide; D003913:Dextroamphetamine