Methamphetamine neurotoxicity and striatal glutamate release: comparison to 3, 4-methylenedioxymethamphetamine

Nash, John J.; Yamamoto, Bryan K.

doi:10.1016/0006-8993(92)90713-j

Cited by 337 publications

(223 citation statements)

References 34 publications

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“…2). 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: 83%

“…The neurotoxic effects are evidenced by long-term depletions in striatal dopamine (DA) and serotonin (5-HT) concentrations, and their uptake sites (Friedman et al, 1998;Ricaurte et al, 1982;Wagner et al, 1980), decreases in tryptophan and tyrosine hydroxylase activity (Bakhit et al, 1981), and cell loss (Deng et al, 2007;Sonsalla et al, 1996;Thiriet et al, 2005;Yu et al, 2004;Zhu et al, 2006). In addition to the hypotheses of oxidative stress and apoptosis as mechanisms of METH-induced neurotoxicity (for review, see Davidson et al, 2001;Kita et al, 2003;Quinton and Yamamoto, 2006), increases in the extracellular concentrations of glutamate (GLU) have been also suggested to play an important role (Abekawa et al, 1994;Nash and Yamamoto, 1992;Sonsalla et al, 1989;Stephans and Yamamoto, 1994). Recently, it has been demonstrated that spectrin proteolysis resulting from the activation of ionotropic GLU receptors, influx of Ca 2+ , and the subsequent activation of the calcium-dependent protease, calpain (Siman et al, 1989), is increased after METH administration (Staszewski and Yamamoto, 2006).…”

Section: Introductionmentioning

confidence: 99%

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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: 83%

Section: Introductionmentioning

confidence: 99%

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

Tata

Yamamoto

2008

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“…In fact a variety of neurotransmitters are released under METH administration - namely, serotonin [66] glutamate [67-69] and acetylcholine [70, 71]. Among these, catecholamine neurons are considered as the main target since METH is a powerful DA and NE releaser [72, 73].…”

Section: Molecular Effects Of Methamphetamine (Meth) On Catecholaminementioning

confidence: 99%

“…It is likely that METH-induced glutamate release in limbic brain regions may reach the threshold to trigger convulsive seizures in the absence of endogenous NE. In fact, METH is a powerful glutamate releaser [67-69], while NE is considered to be a pivotal endogenous seizure suppressive mechanism [20, 140-143]. …”

Section: The Role Of Ne In Methamphetamine-induced Behavioural Changesmentioning

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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“…Whereas repeated cocaine administration produces robust drug-induced glutamate sensitization within the NAC [e.g., 31,35,47,57], repeated dosing with non-toxic regimens of amphetamine or methamphetamine elicits little effect upon the capacity of these drugs to alter glutamate levels within the corticoaccumbens pathway [61,272]. In contrast, repeated high dose amphetamine or methamphetamine regimens that induce dopamine neurotoxicity produce an increase in glutamate content within the PFC [273], a delayed increase in dorsal and ventral striatal glutamate levels [60,[274][275][276][277] and enhance potassium-stimulated, but not methamphetaminestimulated, glutamate release within the PFC [277]. Whether or not the more modest effects of amphetamine regimens upon corticoaccumbens glutamate relate to the duration of withdrawal remains to be determined.…”

Section: Homers and Methamphetaminementioning

confidence: 99%

Homers regulate drug-induced neuroplasticity: Implications for addiction

Szumlinski

Ary

Lominac

2008

Biochemical Pharmacology

118

160

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Drug addiction is a chronic, relapsing disorder, characterized by an uncontrollable motivation to seek and use drugs. Converging clinical and preclinical observations implicate pathologies within the corticolimbic glutamate system in the genetic predisposition to, and the development of, an addicted phenotype. Such observations pose cellular factors regulating glutamate transmission as likely molecular candidates in the etiology of addiction. Members of the Homer family of proteins regulate signal transduction through, and the trafficking of, glutamate receptors, as well as maintain and regulate extracellular glutamate levels in corticolimbic brain regions. This review summarizes the existing data implicating the Homer family of protein in acute behavioral and neurochemical sensitivity to drugs of abuse, the development of drug-induced neuroplasticity, as well as other behavioral and cognitive pathologies associated with an addicted state.

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Methamphetamine neurotoxicity and striatal glutamate release: comparison to 3, 4-methylenedioxymethamphetamine

Cited by 337 publications

References 34 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

The Effects of Locus Coeruleus and Norepinephrine in Methamphetamine Toxicity

Homers regulate drug-induced neuroplasticity: Implications for addiction

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