Influence of methamphetamine on nigral and striatal tyrosine hydroxylase activity and on striatal dopamine levels

Kogan, Frederick J.; Nichols, William K.; Gibb, James W.

doi:10.1016/0014-2999(76)90090-x

Cited by 209 publications

(124 citation statements)

References 22 publications

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“…It has been well documented that AMPH and METH produce selective depletions of striatal DA and/or 5-HT in the rat (Kogan et al, 1976, Wagner et al, 1980 and that MDMA produces a selective long-term depletion of 5-HT (Schmidt, 1987, Battaglia et al, 1988. In the present study, repeated administration of PMA also resulted in a selective depletion of striatal 5-HT.…”

Section: Discussionsupporting

confidence: 68%

“…Results from studies in humans, non-human primates and rodents support the view that these compounds cause structural damage to monoamine nerve terminals and are thereby neurotoxic (O'Callaghan, 2002a, Lyles and Cadet, 2003, Itzhak and Achat-Mendes, 2004. Such data include the finding that repeated high-dose administration of METH results in a reduction in striatal dopamine (DA) and serotonin (5-HT) concentrations (Kogan et al, 1976, Wagner et al, 1980, a decrease in the activity of tyrosine and tryptophan hydroxylase, the rate-limiting enzymes responsible for the production of DA and 5-HT (Hotchkiss and Gibb, 1980), and reduced number of amine uptake sites (Wagner et al, 1980). Likewise, repeated high-dose administration of MDMA produces selective, long-term reductions in striatal 5-HT concentration (Schmidt, 1987, Battaglia et al, 1988, tryptophan hydroxylase activity (Stone et al, 1986, Schmidt and Taylor, 1987, Stone et al, 1987 and the number of 5-HT reuptake sites (Battaglia et al, 1987).…”

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confidence: 94%

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The effect of amphetamine analogs on cleaved microtubule-associated protein-tau formation in the rat brain

et al. 2007

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The present study quantified the cleaved form of the microtubule associated protein tau (cleaved MAP-tau, C-tau), a previously demonstrated marker of CNS toxicity, following the administration of monoamine-depleting regimens of the psychostimulant drugs amphetamine (AMPH), methamphetamine (METH), ±3,4-methylenedioxymethamphetamine (MDMA), or paramethoxyamphetamine (PMA) in an attempt to further characterize psychostimulant-induced toxicity. A dopamine (DA)-depleting regimen of AMPH produced an increase in C-tau immunoreactivity in the striatum, while a DA-and serotonin (5-HT)-depleting regimen of METH produced an increase in the number of C-tau immunoreactive cells in the striatum and CA2/CA3 and dentate gyrus regions of the hippocampus. MDMA and PMA, two psychostimulant drugs that produce selective 5-HT depletion in the striatum, had no effect on C-tau immunoreactivity in the striatum or hippocampus. Furthermore, 5,7-dihydroxytryptamine (5,7-DHT), an established 5-HT selective neurotoxin, did not produce an increase in C-tau immunoreactivity. Dual fluorescent immunocytochemistry with antibodies to GFAP and C-tau indicated that C-tau immunoreactivity was present in astrocytes, not neurons, suggesting that increased C-tau may be an alternative indicator of reactive gliosis. The present results are consistent with previous findings that the DA-depleting psychostimulants AMPH and METH produce reactive gliosis whereas the 5-HT-depleting drugs MDMA and PMA, as well as the known 5-HT selective neurotoxin 5,7-DHT, do not produce an appreciable glial response. Keywords methamphetamine; 3,4-methylenedioxymethamphetamine; amphetamine; paramethoxyamphetamine; 5,7-dihydroxytryptamine; toxicity Methamphetamine (METH) and ±3,4-methylenedioxymethamphetamine (MDMA) are substituted phenylethylamines whose popularity among young adults continues to be a public

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Section: Discussionsupporting

confidence: 68%

mentioning

confidence: 94%

The effect of amphetamine analogs on cleaved microtubule-associated protein-tau formation in the rat brain

et al. 2007

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“…Level of dynorphin B, a cotransmitter released with excitation, was doubled in the neostriatum and substantia nigra. Prolonged exposure to MA has neurotoxic effects on striatal cells via both apoptotic (Cadet et al, 2003) and neurotoxic mechanisms (Davidson et al, 2001) associated with a marked decrease in tyrosine hydroxylase activity, dopamine, and dopamine transporter (DAT) binding sites in the striatum (Kogan et al, 1976;Gibb et al, 1990). The acute neurochemical effects of MA appear to be mediated by a precipitous rise in postsynaptic dopamine, with relative activation of the direct circuit via GLU and altered cotransmitter release.…”

Section: Ma-induced Alterations In Neurochemistry Preclinical Studiesmentioning

confidence: 99%

Do Preclinical Findings of Methamphetamine-Induced Motor Abnormalities Translate to an Observable Clinical Phenotype?

Caligiuri

Buitenhuys

2005

Neuropsychopharmacol

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This review summarizes the preclinical literature of the effects of methamphetamine (MA) on subcortical dopaminergic and GABAergic mechanisms underlying motor behavior with the goal of elucidating the clinical presentation of human MA-induced movement disorders. Acute and chronic MA exposure in laboratory animal can lead to a variety of motor dysfunctions including increased locomotor activity, stereotypies, diminished or enhanced response times, and parkinsonian-like features. With the exception of psychomotor impairment and hyperkinesia, MA-induced movement disorders are not well documented in humans. This review attempts to draw parallels between the animal and human changes in basal ganglia neurochemistry associated with MA exposure and offers explanations for why a parkinsonian phenotype is not apparent among individuals who use and abuse MA. Significant differences in the expression of neurotoxicity and presence of multiple environmental and pharmacologic confounds may account for the lack of a parkinsonian phenotype in humans despite evidence of altered dopamine function.

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“…Initial reports on the neurotoxic potential of METH on dopaminergic neurons came from studies in rats (20) and monkeys (21). Anatomical evidence supporting the neurotoxic effects of METH stems from studies showing that a high dose of METH given to rats caused degeneration of DA nerve fibers, loss of tyrosine hydroxylase, DA transporter, tryptophan hydroxylase, and loss of 5-HT-immunoreactive axons and axon terminals (5,6,22).…”

Section: Animal Studiesmentioning

confidence: 99%

Methamphetamine and MDMA (Ecstasy) Neurotoxicity: 'of Mice and Men'

Itzhak¹,

Achat-Mendes²

2004

IUBMB Life

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SummaryMethamphetamine (METH) and 3,4-meythylenedioxymethamphetamine (MDMA; 'ecstasy') are currently major drugs of abuse. One of the major concerns of amphetamines abuse is their potential neurotoxic effect on dopaminergic and serotonergic neurons. Although data from human studies are somewhat limited, compelling evidence suggests that these drugs cause neurotoxicity in rodents and primates. Recent studies in transgenic and knockout mice identified the role of dopamine transporters, nitric oxide, apoptotic proteins, and inflammatory cytokines in amphetamines neurotoxicity. Further research into the mechanisms underlying the dopaminergic and serotonergic neurotoxicity and the behavioral corollaries of these neuronal insults could facilitate our understanding of the consequences of human abuse of METH and MDMA on cognition, drug-seeking behavior, extinction and relapse. IUBMB Life, 56: 249-255, 2004

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Influence of methamphetamine on nigral and striatal tyrosine hydroxylase activity and on striatal dopamine levels

Cited by 209 publications

References 22 publications

The effect of amphetamine analogs on cleaved microtubule-associated protein-tau formation in the rat brain

The effect of amphetamine analogs on cleaved microtubule-associated protein-tau formation in the rat brain

Do Preclinical Findings of Methamphetamine-Induced Motor Abnormalities Translate to an Observable Clinical Phenotype?

Methamphetamine and MDMA (Ecstasy) Neurotoxicity: 'of Mice and Men'

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