Reciprocal changes in striatal dopamine and ?-phenylethylamine induced by reserpine in the presence of monoamine oxidase inhibitors

Abstract

Recent studies have demonstrated that selective monoamine oxidase inhibition may induce changes in brain beta-phenylethylamine availability following lesions. The present study used this approach to re-assess the possible effects of reserpine on striatal concentrations of beta-phenylethylamine and of other amines and selected metabolites. Mice were injected with pargyline (2,200 mg kg-1, 4 h), clorgyline (2 mg kg-1, 2 h) or (-)deprenyl (2 mg kg-1, 2 h) alone or in combination with reserpine (1, 10 mg kg-1, 2 h). Increases in beta-phenylethylamine accumulation were observed in the presence of both (-)deprenyl or pargyline respectively after reserpine except in the case of combined 200 mg kg-1 of pargyline plus 1 mg kg-1 of reserpine. In this condition, a minimal dopamine decrease was observed (to 80% of the concentration of pargyline-treated controls). Increases in beta-phenylethylamine concentration were not observed with reserpine alone (1 or 10 mg kg-1). In the latter condition, the concentrations of beta-phenylethylamine remained at control values due to the activity of monoamine oxidase B. Changes in p-tyrosine, 5-hydroxytryptamine or tryptophan did not consistently accompany increases in beta-phenylethylamine accumulation. Increased beta-phenylethylamine accumulation was always accompanied by the decreases in dopamine induced by reserpine in mice with either non-selective (200 mg kkg-1 pargyline) or type B monoamine oxidase inhibition (2 mg kg-1 pargyline or deprenyl). These data suggest that although the changes in beta-phenylethylamine accumulation may not be due simply to p-tyrosine availability they are related to dopamine levels in the intact striatum.

Trace Amines and Their Receptors

“…Likewise, no effect of depolarization on TRP release from striatal slices was Trace Amines and Their Receptors present (Dyck, 1989). The lack of effect of K + -induced depolarization strongly suggests that these compounds are neither stored in synaptic vesicles nor released by exocytosis, presumably indicating "release" by simple diffusion across the membrane, consistent with previous reports of a lack of reserpine-sensitive vesicular storage (Juorio et al, 1988). In contrast, veratridine-induced depolarization does increase the release of TYR from striatal slices (Dyck, 1989), although whether similar effects occur with PEA and/or TRP was not studied.…”

MONOAMINE OXIDASE: From Genes to Behavior

“…Both MAO A-deficient mice (Cases et al 1995) and MAO B-deficient mice (Grimsby et al 1997) show an increased reactivity to stress in the forced-swim test. As NE and DA mediate the stress response and their action is potentiated by PEA (Berry et al 1994Dyck et al 1993, Juorio et al 1988, Paterson et al 1990, Yu et al 1994, these findings are consistent with elevated brain levels of NE and DA in MAO A KO mice (Cases et al 1995) and PEA in MAO B KO mice (Grimsby et al 1997).…”

Substances increasing the extracellular content of dopamine in the striatum prevent the development of haloperidol catalepsy in rats

“…It is well known that the extracellular DA concentration can be increased in the striatum in the following ways: by boosting transmitter release (the potential-dependent one by blocking the terminal DA autoreceptors, of heteroreceptor influence; the potential-independent one by substances releasing DA with the aid of a carrier), by blocking the monoarnine reuptake, activating biosynthesis, and by inhibiting monoamine oxidase (MAO) activity [4,5,9,10,15]. Accordingly, the following substances were used for the study: sulpiride, an inhibitor of the terminal DA autoreceptors, which induces an additional increase of DA release in the rat striatum against the background of haloperidol [6]; piracetam, which boosts DA release in the striatum as a result of probable action on the glutamate receptors and involvement in the processes of heteroreceptor regulation [ 1]; amphetamine, which releases newly synthesized cytoplasmic DA as a result of an tetrodotoxin-insensitive process with the aid of a carrier [15], nomifenzine, an inhibitor of monoamine reuptake [5]; L-DOPA, a DA precursor [10]; and pargyline, an MAO inhibitor [9].…”

“…Accordingly, the following substances were used for the study: sulpiride, an inhibitor of the terminal DA autoreceptors, which induces an additional increase of DA release in the rat striatum against the background of haloperidol [6]; piracetam, which boosts DA release in the striatum as a result of probable action on the glutamate receptors and involvement in the processes of heteroreceptor regulation [ 1]; amphetamine, which releases newly synthesized cytoplasmic DA as a result of an tetrodotoxin-insensitive process with the aid of a carrier [15], nomifenzine, an inhibitor of monoamine reuptake [5]; L-DOPA, a DA precursor [10]; and pargyline, an MAO inhibitor [9].…”

“…A. Romanov, Member of the Russian Academy of Medical Sciences} cholinesterase poisons may occur on a mass scale during accidents at chemical plants, specifcally, at those engaged in the destruction of toxic OPC. Recently many publications have appeared that are devoted to studies of the immunotoxic effects of OPC [2,3,5,9]. The principal mechanisms of these effects have been disclosed [5], thus permitting a targeted pharmacological correction of postintoxication immunodeficiency in order to prevent various infectious complications and diseases.…”