Striatal subregions are differentially vulnerable to the neurotoxic effects of methamphetamine

Eisch, Amelia J.; Gaffney, Mary Kathryn; Weihmuller, Fredric B.; O’Dell, Steven J.; Marshall, John F.

doi:10.1016/0006-8993(92)90201-j

Cited by 108 publications

(80 citation statements)

References 33 publications

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“…Therefore, it appears that drug dispositional changes may occur only when METH pretreatment and/or binge doses are relatively high. Furthermore, particularly when lower doses have been used, the degree of protection has often appeared to be not only brain region-and transmitter-dependent, but also dependent on the specific measure of neurotransmitter function (Segal and Kuczenski, 1987;Eisch et al, 1992;Eisch and Marshall, 1998;Friedman et al, 1998;Wilson et al, 1994;Chapman et al, 2001). Thus, for example, when tested subsequent to the binge, whereas both basal DA and the stimulant-induced extracellular DA response are attenuated by an acute binge (Cass and Manning, 1999), only basal DA is protected when the binge is preceded by ED pretreatment (Segal and Kuczenski, 1997a, b, c;Kuczenski and Segal, 1997).…”

Section: Discussionmentioning

confidence: 99%

“…Multiple injections are administered within a day, typically at 2-h intervals, to simulate the prolonged elevation of drug associated with binge-pattern administration in humans. Although several variations in this procedure have been studied, most researchers have reported a 'neurotoxic' profile which, especially at the higher doses, includes regionally specific damage to DA terminals as well as profound, although less persistent, changes in other neurotransmitter systems (Seiden and Ricaurte, 1987;Eisch et al, 1992;Axt et al, 1994;Bowyer and Holson, 1995;Pu and Vorhees, 1995;Cass, 1997;Fleckenstein et al, 2000;O'Callaghan and Miller, 2000). The mechanisms underlying these changes have received considerable attention, with many studies suggesting important roles for temperature and accumulation of reactive oxidative species, as well as other factors, in the cascade of changes that appear to result from this high-dose 'binge' protocol (Farfel and Seiden, 1994;Seiden and Sabol, 1995;Stephans and Yamamoto, 1996;Wrona et al, 1997;Xie et al, 2000;Davidson et al, 2001;Yuan et al, 2001;Larsen et al, 2002).…”

Section: Introductionmentioning

confidence: 99%

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Escalating Dose Methamphetamine Pretreatment Alters the Behavioral and Neurochemical Profiles Associated with Exposure to a High-Dose Methamphetamine Binge

Segal

Kuczenski

O'Neil

et al. 2003

Neuropsychopharmacol

105

108

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The neurotoxic effects of methamphetamine (METH) have been characterized primarily from the study of high-dose binge regimens in rodents. However, this drug administration paradigm does not include a potentially important feature of stimulant abuse in humans, that is, the gradual escalation of stimulant doses that frequently occurs prior to high-dose exposure. We have argued that pretreatment with escalating doses (EDs) might significantly alter the neurotoxic profile produced by a single high-dose binge. In the present study, we tested this hypothesis by pretreating rats with saline or gradually increasing doses of METH (0.1-4.0 mg/kg over 14 days), prior to an acute METH binge (4 Â 6 mg/kg at 2 h intervals). These animals, whose behavior was continuously monitored throughout drug treatment, were then killed 3 days later for determination of caudate-putamen dopamine (DA) content, levels of [ We suggest that further study of the effects produced by a regimen which includes a gradual escalation of doses prior to high-dose METH binge exposure could more accurately identify the neurochemical and behavioral changes relevant to those that occur as a consequence of high-dose METH abuse in humans.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Escalating Dose Methamphetamine Pretreatment Alters the Behavioral and Neurochemical Profiles Associated with Exposure to a High-Dose Methamphetamine Binge

Segal

Kuczenski

O'Neil

et al. 2003

Neuropsychopharmacol

105

108

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“…Rather unexpectedly, although the NK-1 receptor blockade did not display protection on the 3rd and 7th day post-treatment, it also rescued METH-induced loss of DAT sites in NAc on the 14th and 28th day after treatment, suggesting the presence of both immediate and delayed neurotoxic reactions that contribute to long-term toxic effects induced by METH exposure. It is well known that NAc is more resistant to METH toxicity (Eisch et al 1992), but the mechanism underlying the regional heterogeneity of METH has not yet been elucidated. The dopamine transporter is believed to be an essential component of pathway leading to METH toxicity in the striatum (Fumagalli et al 1998).…”

Section: Discussionmentioning

confidence: 99%

Neurokinin‐1 (NK‐1) receptor antagonists abrogate methamphetamine‐induced striatal dopaminergic neurotoxicity in the murine brain

Cadet

Angulo

2002

Journal of Neurochemistry

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Methamphetamine (METH) is an addictive substance that also causes extensive neural degeneration in the central nervous system. Because METH augments striatal substance P (SP) levels, we hypothesized that this neuropeptide plays a role in methamphetamine-induced toxicity and neural damage in the striatum. In this study we present evidence demonstrating that signaling through the neurokinin-1 (NK-1) receptor by SP plays an important role in methamphetamine-induced toxicity in the striatum. We tested the effects of the selective NK-1 receptor antagonists WIN-51,708 and L-733,060 on several markers of dopaminergic terminal toxicity in the mouse striatum. Administration of NK-1 receptor antagonist prevented the loss of dopamine transporters assessed by autoradiography and western blotting, the loss of tissue dopamine assessed by high-pressure liquid chromatography, and the loss of tyrosine hydroxylase, as well as the induction of glial fibrillary acidic protein determined by western blotting. Pre-treatment with NK-1 receptor antagonist had no effect on METH-induced hyperthermia. Pre-exposure of mice to either of the NK-1 receptor antagonists alone was without effect on all of these neurochemical markers. These results provide the first evidence that tachykinins, particularly SP, acting through NK-1 receptors, play a crucial role in the pathogenesis of nigrostriatal dopaminergic terminal degeneration induced by METH. This finding could lead to novel therapeutic strategies to offset drug addictions as well as in the treatment of a number of disorders including Parkinson's and Huntington's diseases.

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“…In both mice and rats, acute repeated injections of METH produce long-lasting decreases in DA levels [145, 149-153], and long-term reductions in several DA markers, such as TH [144, 154, 155], DAT [152, 156, 157], and VMAT-2 [155, 157-159] within the striatum. Morphological studies demonstrate that the persistent loss of integrity of DA biochemical markers is due to the degeneration of DA axon terminals [145-149].…”

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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Striatal subregions are differentially vulnerable to the neurotoxic effects of methamphetamine

Cited by 108 publications

References 33 publications

Escalating Dose Methamphetamine Pretreatment Alters the Behavioral and Neurochemical Profiles Associated with Exposure to a High-Dose Methamphetamine Binge

Escalating Dose Methamphetamine Pretreatment Alters the Behavioral and Neurochemical Profiles Associated with Exposure to a High-Dose Methamphetamine Binge

Neurokinin‐1 (NK‐1) receptor antagonists abrogate methamphetamine‐induced striatal dopaminergic neurotoxicity in the murine brain

The Effects of Locus Coeruleus and Norepinephrine in Methamphetamine Toxicity

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