Ontogeny of methamphetamine-induced neurotoxicity and associated hyperthermic response

Cappon, Gregg D.; Morford, LaRonda L.; Vorhees, Charles V.

doi:10.1016/s0165-3806(97)81791-9

Cited by 80 publications

(78 citation statements)

References 36 publications

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“…We demonstrated increased GFAP in the neostriatum and decreased monoamines at 72 h after MA administration in both the neostriatum and hippocampus as have others (Bowyer et al, 1994;Cappon et al, 1997;O'Callaghan and Miller, 2002;O'Dell and Marshall, 2002). Given that brain monoamines were reduced 3 days post-treatment and were still reduced (albeit to a somewhat lesser degree) at the end of behavioral testing 2 months later, these data taken together indicate that monoamines were reduced throughout the course of the behavioral experiment; raising the question of whether these reductions mediate the behavioral changes.…”

Section: Discussionsupporting

confidence: 89%

Effect of (+)-methamphetamine on path integration learning, novel object recognition, and neurotoxicity in rats

et al. 2008

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Rationale-Methamphetamine (MA) has been implicated in cognitive deficits in humans after chronic use. Animal models of neurotoxic MA exposure reveal persistent damage to monoaminergic systems, but few associated cognitive effects.Objectives-Since, questions have been raised about the typical neurotoxic dosing regimen used in animals and whether it adequately models human cumulative drug exposure, these experiments examined two different dosing regimens.Methods-Rats were treated with one of two regimens, one the typical neurotoxic regimen (4 × 10 mg/kg every 2 h) and one based on pharmacokinetic modeling (Cho et al. 2001) designed to better represent accumulating plasma concentrations of MA as seen in human users (24 ×1.67 mg/kg once every 15 min); matched for total daily dose. In two separate experiments, dosing regimens were compared for their effects on markers of neurotoxicity or on behavior.Results-On markers of neurotoxicity, MA showed decreased DA and 5-HT, and increased glial fibrillary acidic protein and increased corticosterone levels regardless of dosing regimen 3 days posttreatment. Behaviorally, MA-treated groups, regardless of dosing regimen, showed hypoactivity, increased initial hyperactivity to a subsequent MA challenge, impaired novel object recognition, impaired learning in a multiple-T water maze test of path integration, and no differences on spatial navigation or reference memory in the Morris water maze. After behavioral testing, reductions of DA and 5-HT remained.Conclusions-MA treatment induces an effect on path integration learning not previously reported. Dosing regimen had no differential effects on behavior or neurotoxicity.

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Section: Discussionsupporting

confidence: 89%

Effect of (+)-methamphetamine on path integration learning, novel object recognition, and neurotoxicity in rats

et al. 2008

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“…5-MEO-DIPT or SAL was administered four times at 2-h intervals on a single day (ie, the entire dosing period was 6 h from first to last dose). The multiple dose regimen is consistent with drug administration paradigms for other psychostimulants (Cappon et al, 1997;Cohen et al, 2005;Farfel and Seiden, 1995;O'Callaghan and Miller, 2002;O'Dell and Marshall, 2002). Injections were applied subcutaneously in the dorsum and the injection sites were varied to prevent irritation to the dermis, although some minor irritation was observed.…”

Section: -Meo-dipt Administrationmentioning

confidence: 86%

“…For example, markers for neurotoxicity are increased and monoamines decreased 72 h following a single day of multiple methamphetamine administrations (Bowyer et al, 1994;Cappon et al, 1997;O'Callaghan and Miller, 2002;O'Dell and Marshall, 2002). We therefore selected the 72 h time point for examination of brain regions in this study.…”

Section: Effects Of 5-meo-diptmentioning

confidence: 99%

Alterations in Body Temperature, Corticosterone, and Behavior Following the Administration of 5-Methoxy-Diisopropyltryptamine (‘Foxy’) to Adult Rats: a New Drug of Abuse

Williams

Herring

Schaefer

et al. 2006

Neuropsychopharmacol

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Many drugs are used or abused in social contexts without understanding the ramifications of their use. In this study, we examined the effects of a newly popular drug, 5-methoxy-diisopropyltryptamine (5-MEO-DIPT; 'foxy' or 'foxy-methoxy'). Two experiments were performed. In the first, 5-MEO-DIPT (0, 10, or 20 mg/kg) was administered to rats four times on a single day and animals were examined 3 days later. The animals that received 5-MEO-DIPT demonstrated hypothermia during the period of drug administration and delayed mild hyperthermic rebound for at least 48 h. Corticosterone levels in plasma were elevated in a dose-dependent manner compared to saline-treated animals with minor changes in 5-HT turnover and no changes in monoamine levels. In experiment 2, rats were examined in behavioral tasks following either 0 or 20 mg/kg of 5-MEO-DIPT. The animals treated with 5-MEO-DIPT showed hypoactivity and an attenuated response to ( + )-methamphetamine-induced stimulation (1 mg/kg). In a test of path integration (Cincinnati water maze), 5-MEO-DIPT-treated animals displayed deficits in performance compared to the saline-treated animals. No differences were noted in the ability of the animals to perform in the Morris water maze or on tests of novel object or place recognition. The data demonstrate that 5-MEO-DIPT alters the ability of an animal to perform certain cognitive tasks, while leaving others intact and disrupts the endocrine system. 5-MEO-DIPT may have the potential to induce untoward effects in humans.

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“…Bowyer et al (1994) and others (Fukumura et al, 1998) have shown that MA-induced hyperthermia is correlated with neurotransmitter reduction in the adult, but not in the developing rat. Cappon et al (1997) argued that induction of hyperthermia is a requisite for the expression of MA-induced striatal dopamine neurotoxicity. There is some evidence that DAT may play an important role in the expression of MA-induced hyperthermia and neurotoxicity (Xie et al, 2000;Broening et al, 2005).…”

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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Ontogeny of methamphetamine-induced neurotoxicity and associated hyperthermic response

Cited by 80 publications

References 36 publications

Effect of (+)-methamphetamine on path integration learning, novel object recognition, and neurotoxicity in rats

Effect of (+)-methamphetamine on path integration learning, novel object recognition, and neurotoxicity in rats

Alterations in Body Temperature, Corticosterone, and Behavior Following the Administration of 5-Methoxy-Diisopropyltryptamine (‘Foxy’) to Adult Rats: a New Drug of Abuse

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

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