Dopamine uptake inhibitors block long-term neurotoxic effects of methamphetamine upon dopaminergic neurons

Marek, Gerard J.; Vosmer, Georgetta; Seiden, Lewis S.

doi:10.1016/0006-8993(90)90467-p

Cited by 119 publications

(108 citation statements)

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“…This effect is perhaps due to a decrease in DA transport (Eisch et al 1996;Fleckenstein et al 1997), required for Meth to be taken up to elicit its effect on DA terminals (Marek et al 1990). The most striking effect of repeated Meth was, however, on K + -evoked inhibitory (GABA) and excitatory (Glu, Asp) amino acid levels, which were increased.…”

Section: Discussionmentioning

confidence: 99%

“…Furthermore, while, as measured by quantitative autoradiography, the neurotoxic effect of Meth is seen in widespread brain regions receiving monoamine terminals, the cell body regions are largely unaffected (Brunswick et al 1992). It has been proposed that the long-term effects of Meth depend on the amount of overflow of DA induced by the drug (O'Dell et al 1991), and, in agreement, it has been shown that Meth-induced damage is prevented by inhibition of DA synthesis (Gibb and Kogan 1979;Hotchkiss and Gibb 1980;, DA transport Marek et al 1990), or even by DA receptor antagonism (Sonsalla et al 1986;O'Dell et al 1993). It has been argued, however, that Meth may also increase glutamate (Glu) overflow (Sonsalla et al 1989;Nash and Yamamoto 1992;Stephans and Yamamoto 1994), leading to the hypothesis that there is a synergism between both DA and Glu release, and that this is a requirement for Meth-induced neurotoxicity (Abekawa et al 1994;Eisch et al 1996).…”

mentioning

confidence: 87%

“…There is evidence that high or repeated doses of d-N, a-dimethylphenylethylamine (methamphetamine, Meth) induce long-term deficits in basal ganglia neurotransmission, both in rodents and humans, mainly affecting the monoamines dopamine (DA; Fibiger and McGeer 1971;Seiden et al 1976;Ricaurte et al 1980;Marek et al 1990) and serotonin (5-hydroxytryptamine, 5-HT; Ricaurte et al 1980;Haughey et al 2000), but also amino acids (Sonsalla et al 1989;Nash and Yamamoto 1992;Marshall et al 1993;Abekawa et al 1994;Meshul 1997, 1999) and neuropeptides (Castel et al 1994;Smith and McGinty 1994;McGinty 1995, 1996;Alburges et al 2001aAlburges et al , 2001b. The long-term effects of Meth are largely restricted to the nigrostriatal DA system (Ricaurte et al 1980;Marshall and Navarrete 1990;Marshall et al 1993;Burrows and Meshul 1997).…”

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confidence: 99%

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Effect of single and repeated methamphetamine treatment on neurotransmitter release in substantia nigra and neostriatum of the rat

Bustamante

You²,

Castel

et al. 2002

Journal of Neurochemistry

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The main purpose of this study was to characterize the initial neurotransmission cascade elicited by methamphetamine, analysing simultaneously with in vivo microdialysis monoamine, amino acid and neuropeptide release in substantia nigra and neostriatum of the rat. The main effect of a single systemic dose of methamphetamine (15 mg/kg, subcutaneously) was an increase in dopamine levels, both in substantia nigra ( 10-fold) and neostriatum ( 40-fold), accompanied by a significant, but lesser, increase in dynorphin B ( two-fold, in both regions), and a decrease in monoamine metabolites. A similar effect was also observed after local administration of methamphetamine (100 lM) via the microdialysis probes, but restricted to the treated region. In other experiments, rats were repeatedly treated with methamphetamine or saline, with the last dose administered 12 h before microdialysis. Dopamine K + -stimulated release was decreased following repeated methamphetamine administration compared with that following saline, both in the substantia nigra (by 65%) and neostriatum (by 20%). In contrast, the effect of K + -depolarization on glutamate, aspartate and GABA levels was increased following repeated administration of methamphetamine. In conclusion, apart from an impairment of monoamine neurotransmission, repeated methamphetamine produces changes in amino acid homeostasis, probably leading to NMDA-receptor overstimulation.

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Section: Discussionmentioning

confidence: 99%

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confidence: 87%

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confidence: 99%

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Effect of single and repeated methamphetamine treatment on neurotransmitter release in substantia nigra and neostriatum of the rat

Bustamante

You²,

Castel

et al. 2002

Journal of Neurochemistry

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“…In fact, overexpression of VMAT2, which stores DA in the vesicles, significantly protects PC12 against METH toxicity [165], while a mutant strain of mice, which possesses only 5-10% of the VMAT2 expressed by wild-type animals, undergo enhanced METH-induced striatal neurotoxicity [166]. For the same reasons, DAT inhibitors protect against METH-induced striatal DA damage [74, 83, 167]. Similar protective effects have been described in the striatum of DAT KO mice [168].…”

Section: Methamphetamine-induced Dopaminergic Toxicitymentioning

confidence: 99%

The Effects of Locus Coeruleus and Norepinephrine in Methamphetamine Toxicity

Ferrucci

Giorgi

Bartalucci

et al. 2013

Current Neuropharmacology

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The activity of locus coeruleus (LC) neurons has been extensively investigated in a variety of behavioural states. In fact this norepinephrine (NE)-containing nucleus modulates many physiological and pathological conditions including the sleep-waking cycle, movement disorders, mood alterations, convulsive seizures, and the effects of drugs such as psychostimulants and opioids. This review focuses on the modulation exerted by central NE pathways on the behavioural and neurotoxic effects produced by the psychostimulant methamphetamine, essentially the modulation of the activity of mesencephalic dopamine (DA) neurons. In fact, although NE in itself mediates some behavioural effects induced by methamphetamine, NE modulation of DA release is pivotal for methamphetamine-induced behavioural states and neurotoxicity. These interactions are discussed on the basis of the state of the art of the functional neuroanatomy of central NE- and DA systems. Emphasis is given to those brain sites possessing a remarkable overlapping of both neurotransmitters.

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“…Bupropion's ability to block the DA transporter (Meyer et al, 2002) may help restore dopaminergic homeostasis by increasing intrasynaptic DA. Bupropion pretreatment has been shown to protect against acute methamphetamine-induced decreases in DA uptake in striatal synaptosomes (Kim et al, 2000), and in vivo, to reduce the neurotoxic effects produced in rats by a single large dose (100 mg/kg, s.c.) of methamphetamine (Marek et al, 1990).…”

Section: Introductionmentioning

confidence: 99%

Bupropion for the Treatment of Methamphetamine Dependence

Elkashef

Rawson

Anderson

et al. 2007

Neuropsychopharmacol

199

188

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Bupropion was tested for efficacy in increasing weeks of abstinence in methamphetamine-dependent patients, compared to placebo. This was a double-blind placebo-controlled study, with 12 weeks of treatment and a 30-day follow-up. Five outpatient substance abuse treatment clinics located west of the Mississippi participated in the study. One hundred and fifty-one treatment-seekers with DSM-IV diagnosis of methamphetamine dependence were consented and enrolled. Seventy-two participants were randomized to placebo and 79 to sustained-release bupropion 150 mg twice daily. Patients were asked to come to the clinic three times per week for assessments, urine drug screens, and 90-min group psychotherapy. The primary outcome was the change in proportion of participants having a methamphetamine-free week. Secondary outcomes included: urine for quantitative methamphetamine, self-report of methamphetamine use, subgroup analyses of balancing factors and comorbid conditions, addiction severity, craving, risk behaviors for HIV, and use of other substances. The generalized estimating equation regression analysis showed that, overall, the difference between bupropion and placebo groups in the probability of a non-use week over the 12-week treatment period was not statistically significant (p ¼ 0.09). Mixed model regression was used to allow adjustment for baseline factors in addition to those measured (site, gender, level of baseline use, and level of symptoms of depression). This subgroup analysis showed that bupropion had a significant effect compared to placebo, among male patients who had a lower level of methamphetamine use at baseline (po0.0001). Comorbid depression and attention-deficit/ hyperactivity disorder did not change the outcome. These data suggest that bupropion, in combination with behavioral group therapy, was effective for increasing the number of weeks of abstinence in participants with low-to-moderate methamphetamine dependence, mainly male patients, regardless of their comorbid condition.

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Dopamine uptake inhibitors block long-term neurotoxic effects of methamphetamine upon dopaminergic neurons

Cited by 119 publications

References 26 publications

Effect of single and repeated methamphetamine treatment on neurotransmitter release in substantia nigra and neostriatum of the rat

Effect of single and repeated methamphetamine treatment on neurotransmitter release in substantia nigra and neostriatum of the rat

The Effects of Locus Coeruleus and Norepinephrine in Methamphetamine Toxicity

Bupropion for the Treatment of Methamphetamine Dependence

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