The Japanese Journal of Pharmacology
Online ISSN : 1347-3506
Print ISSN : 0021-5198
2-Phenylethylamine and Methamphetamine Enhance the Spinal Monosynaptic Reflex by Releasing Noradrenaline from the Terminals of Descending Fibers
Hideki OnoHiroyuki ItoHideomi Fukuda
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1991 Volume 55 Issue 3 Pages 359-366

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Abstract

Experiments were performed on spinalized rats transected at C1. Intravenous administration of 2-phenylethylamine-HC1 (PEA-HC1) (0.3 and 1 mg/kg, i.v.) and methamphetamine-HC1 (MAP-HC1) (0.1 and 0.3 mg/kg, i.v.) increased the amplitude of the monosynaptic reflex (MSR). The increase of the MSR caused by PEA and MAP was antagonized by prazosin-HC1 and abolished by the pretreatment with reserpine (i.p.) and 6-hydroxydopamine (intracisternally, 14 days previously). A dopamine D1 antagonist, SK&F 83566-HBr (0.01 mg/kg, i.v. ), and a D2 antagonist, YM-09151-2 (0.3 mg/kg, i.v.), did not antagonize the increasing effects produced by PEA and MAP. An inhibitor of type-B monoamine oxidase, (—)deprenyl-HCl (1 mg/kg, i.v.), prolonged the effect of PEA but not that of MAP, suggesting that PEA alone, and not its metabolites, enhanced the MSR. These results suggest that PEA and MAP increase the amplitude of the MSR by releasing noradrenaline from the terminals of descending noradrenergic fibers, and that PEA, an endogenous trace amine, has a mechanism of action similar to that of MAP.

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