High-dose methamphetamine treatment alters presynaptic GABA and glutamate immunoreactivity

Burrows, Kristan B.; Meshul, Charles K.

doi:10.1016/s0306-4522(98)00506-5

Cited by 31 publications

(16 citation statements)

References 71 publications

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“…Extracellular concentrations of GLU in response to METH were similar in duration and magnitude to those reported previously (Abekawa et al, 1994;Nash and Yamamoto, 1992). The current study did not examine the mechanism of the METH-induced increases in striatal GLU, but previous studies showed a D1 receptor-dependent activation of the striatonigral GABAergic pathway (Mark et al, 2004), resulting in a disinhibition of corticostriatal GLUergic projections (Burrows and Meshul, 1999).…”

Section: Discussionsupporting

confidence: 80%

Chronic stress enhances methamphetamine‐induced extracellular glutamate and excitotoxicity in the rat striatum

Tata

Yamamoto

2008

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Striking parallels exist between the neurochemical and toxic effects of stress and methamphetamine. Despite these similarities, no studies have examined how stress may promote the toxic effects of methamphetamine (METH). The current study tested the hypothesis that chronic stress enhances METH toxicity by augmenting glutamate (GLU) release and excitotoxicity in response to METH administration. Adult male Sprague-Dawley rats were exposed to 10 days of unpredictable stress and then received either saline or METH (7.5 mg/kg, i.p., once every 2 h × four injections). Prior exposure to unpredictable stress acutely enhanced the striatal extracellular GLU concentrations in response to METH, and eventually caused proteolysis of the cytoskeleton protein spectrin. Administration of the corticosterone synthesis inhibitor, metyrapone (25 mg/kg, i.p., prior to each stressor), during unpredictable stress attenuated the enhanced striatal GLU release in response to METH, blocked spectrin proteolysis, and attenuated METH-associated toxicity measured by long-term depletions in the dopamine and serotonin tissue content as well as depletions in dopamine and serotonin transporter immunoreactivity of the striatum. In summary, prior exposure to unpredictable stress enhances METH-induced elevations of GLU in the striatum, resulting in long-term excitotoxic damage and an augmentation of damage to dopamine and serotonin terminals. These studies provide a neurochemical basis for how stress contributes to the deleterious effects of METH abuse.

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Section: Discussionsupporting

confidence: 80%

Chronic stress enhances methamphetamine‐induced extracellular glutamate and excitotoxicity in the rat striatum

Tata

Yamamoto

2008

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“…Floran et al (1977) reported that acute MA administration in rats decreased GABA levels via their direct interaction within the striatal dopamine subsystem. Burrows and Meshul (1999) reported striatal and pallidal decreases in GABA immunoreactivity following 1 week of MA exposure; however, GABAergic immunoreactivity increased following prolonged exposure for up to 4 weeks. Prolonged exposure to MA altered presynaptic GABA immunolabeling and increased GLU terminal size in both the striatum and globus pallidus.…”

Section: Ma-induced Alterations In Neurochemistry Preclinical Studiesmentioning

confidence: 93%

“…In rodents, holding the body temperature constant can markedly reduce the toxic effects of MA on the basal ganglia (Burrows and Meshul, 1999). 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.…”

Section: Ma-induced Alterations In Neurochemistry Preclinical Studiesmentioning

confidence: 99%

“…MA exerts powerful effects on several neurochemical systems throughout the brain, including dopamine (Ricaurte et al, 1980(Ricaurte et al, , 1984O'Dell et al, 1993), GABA (Kamata and Kameyama, 1986;Burrows and Meshul, 1999;Bustamante et al, 2002), and GLU (Sonsalla et al, 1989;Nash and Yamamoto, 1992;Abekawa et al, 1994;Burrows and Meshul, 1999). MA is a highly lipophilic monoamine that is capable of entering presynaptic vesicles and competing for resident monoamines causing excessive release postsynaptically (Kuczenski, 1983).…”

Section: Ma-induced Alterations In Neurochemistry Preclinical Studiesmentioning

confidence: 99%

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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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“…Post-embedding immunogold electron microscopy was performed according to the method of Phend et al (1992), with modifications (Meshul et al 1994(Meshul et al , 1995(Meshul et al , 1996a(Meshul et al , 1996bBurrows and Meshul 1999). One block of tissue from each brain region was cut for ultrastructural analysis.…”

Section: Immunocytochemistrymentioning

confidence: 99%

Alterations in nerve terminal glutamate immunoreactivity in the nucleus accumbens and ventral tegmental area following single and repeated doses of cocaine

Kozell

Meshul

2003

Psychopharmacology

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Acute cocaine administration resulted in a significant loss of nerve terminal glutamate immunoreactivity that was persistent in the nucleus accumbens core, but there were only transient changes in the shell. Nerve terminal glutamate immunoreactivities in the behaviorally sensitized and non-sensitized groups were not significantly different from one another, which suggests that cocaine-induced alterations in presynaptic glutamate immunoreactivity may not be sufficient for the expression of behavioral sensitization.

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High-dose methamphetamine treatment alters presynaptic GABA and glutamate immunoreactivity

Cited by 31 publications

References 71 publications

Chronic stress enhances methamphetamine‐induced extracellular glutamate and excitotoxicity in the rat striatum

Chronic stress enhances methamphetamine‐induced extracellular glutamate and excitotoxicity in the rat striatum

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

Alterations in nerve terminal glutamate immunoreactivity in the nucleus accumbens and ventral tegmental area following single and repeated doses of cocaine

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