Ascorbic acid-deficient condition alters central effects of methamphetamine

  title={Ascorbic acid-deficient condition alters central effects of methamphetamine},
  author={Lisa A. Matsuda and Christopher J. Schmidt and James W. Gibb and Glen R. Hanson},
  journal={Brain Research},
Effects of multiple doses of methamphetamine (METH) were examined in normal and ascorbic acid-deficient (scorbutic) guinea pigs. METH-induced decreases of striatal serotonin concentrations were completely antagonized in scorbutic animals. Elevations of nigral substance P-like immunoreactivity also differed significantly in METH-treated scorbutic compared to METH-treated normal animals. Various lines of evidence indicate that dopamine is an essential mediator of METH-induced effects in both… Expand
Effects of methamphetamine on central monoaminergic systems in normal and ascorbic acid-deficient guinea pigs.
In vitro, ascorbic acid increased significantly DA-mediated [3H]5-HT release from striatal slices, thus suggesting a potential role for asCorbate in DA- mediated actions of METH on serotonergic systems. Expand
Exacerbation of methamphetamine-induced neurochemical deficits by melatonin.
Not only did melatonin not prevent METH-induced deficits in serotonergic and dopaminergic parameters, but coadministration of melatonin with METH actually enhanced most of the monoaminergic effects of METH. Expand
Behavioral sensitization to cocaine is not associated with changes in serotonin (5-HT) fiber immunoreactivity in rat forebrain
The hypothesis that unlike some amphetamine derivatives, repeated cocaine administration which results in behavioral sensitization is not neurotoxic to 5-HT axons and terminals in the forebrain is supported. Expand
Effects of high-dose methamphetamine administration on serotonin uptake sites in rat brain measured using [3H]cyanoimipramine autoradiography
The results of this study provide support for the serotonergic neurotoxicity of repeated methamphetamine administration in rats and show that the neurotoxicity is highly regional and dose dependent. Expand
L-ascorbate attenuates methamphetamine neurotoxicity through enhancing the induction of endogenous heme oxygenase-1.
It is concluded that induction of HO-1 expression contributes to the attenuation of METH-induced ROS production and neurotoxicity by Vit. Expand
Are dopamine, norepinephrine, and serotonin precursors of biologically reactive intermediates involved in the pathogenesis of neurodegenerative brain disorders?
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In this communication similarities associated with the neurotoxicity evoked by MPTP, MA and I-R will be reviewed and integrated into a working hypothesis for the underlying neurotoxic mechanisms in which one or more of the neurotransmitters dopamine, norepinephrine and 5-hydroxytryptamine are proposed to be the precursors of biologically reactive intermediates in the pathological processes. Expand
Potential Roles of Accelerated Dopamine Oxidation, Altered Glutathione Metabolism, 5-S-Cysteinyl-Dopamine and its Oxidative Metabolites in the Pathogenesis of Parkinson’s Disease
Many factors appear to be involved in the neurotoxic mechanism that underlies the degeneration of neuromelanin-pigmented dopaminergic neurons in the substantia nigra pars compacta (SNpc) inExpand
Neurotoxic Factors in Parkinson’s Disease and Related Disorders
Preface. Mechanisms of Selective Vulnerability. MPTP/MPP+ Action and Mechanism. Isoquinolines as Potential Neurotoxins. beta-Carbolines as Potential Neurotoxins. Catecholamine-Oxidation Pathways inExpand
From the Alcohol, Drug Abuse, and Mental Health Administration.
Hypophysectomy prior to the onset of puberty was found to drastically reduce the level of PE mRNA in the testis and epididymus, suggesting that pituitary factors affect the expression of the PE gene in these tissues, either directly or indirectly. Expand


Role of dopamine in the neurotoxic effects of methamphetamine.
D dopamine plays an important role in the changes mediated by the administration of methamphetamine in both the dopaminergic and serotonergic systems, and the ability of a single administrations of methamphetamine to depress tryptophan hydroxylase was also dependent on catecholamine synthesis. Expand
Increases of substance P-like immunoreactivity within striatal-nigral structures after subacute methamphetamine treatment.
Substantial increases in the nigral concentration of substance P-like immunoreactivity (SPLI) were observed after subacute administration of the indirect dopamine agonist, methamphetamine (METH, 15Expand
Ascorbic acid and the behavioral response to haloperidol: implications for the action of antipsychotic drugs.
Results suggest that ascorbic acid plays an important role in modulating the behavioral effects of haloperidol and related antipsychotic drugs. Expand
Dopamine-mediated increases in nigral substance P-like immunoreactivity.
The results reported herein strongly suggest that increased dopaminergic and not increased serotonergic activity is responsible for methamphetamine-induced increases in the nigral concentration ofExpand
Ascorbate blocks amphetamine-induced turning behavior in rats with unilateral nigro-striatal lesions
Ascorbate, like other drugs blocking dopamine receptors, attenuated the amphetamine-induced turning behavior and might have a role in regulating dopaminergic transmission and could be of therapeutic value in disorders involving functional dopamine excess. Expand
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Brain and spleen ascorbic acid levels were dramatically decreased, but ethanol preference was not altered by the acute dietary deficiency of this vitamin, and two measures of brain aminergic function (MAO activity and 3H-spiroperidol binding) were not associated with tissue asCorbate levels. Expand
Effect of acute and chronic methamphetamine treatment on tyrosine hydroxylase activity in brain and adrenal medulla.
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Agents which prevent the METH-induced decrease of neostriatal tyrosine hydroxylase activity, i.e., haloperidol, alpha-methyl-p-tyrosine and gamma-aminobutyric acid transaminase inhibitors also prevented the decrease in TPH activity caused by METH. Expand
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It was found that methamphetamine induced changes in regional brain catecholamines, some of which persisted even after the drug was discontinued, and both short and long-term changes in brain cate-cholamines were caused by prolonged administration of methampheta-mine. Expand