Cognitive function and nigrostriatal markers in abstinent methamphetamine abusers

Johanson, Chris E.; Frey, Kirk A.; Lundahl, Leslie H.; Keenan, P. A.; Lockhart, Nancy; Roll, John M.; Galloway, Gantt P.; Koeppe, Robert A.; Kilbourn, Michael R.; Robbins, Trevor W.; Schuster, Charles R.

doi:10.1007/s00213-006-0330-6

Cited by 207 publications

(97 citation statements)

References 41 publications

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“…Similar findings were reported in an earlier PET study using [ 11 C]WIN-35,428, a DAT ligand, including reductions in DAT levels of 23% and 25% respectively in the caudate and putamen of MA abusers who had been abstinent for 3 years on average, relative to controls [97]. A more recent PET study reported a 15% decrease in striatal DAT levels in long-term abstinent MA abusers [106]. The decrease in DAT levels in the striatum of MA abusers has been associated with functional impairments including motor slowing and memory deficits [98].…”

Section: Dopaminergic Transmission and Glucose Metabolism Changes supporting

confidence: 82%

Functional and Structural Brain Changes Associated with Methamphetamine Abuse

2012

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Methamphetamine (MA) is a potent psychostimulant drug whose abuse has become a global epidemic in recent years. Firstly, this review article briefly discusses the epidemiology and clinical pharmacology of methamphetamine dependence. Secondly, the article reviews relevant animal literature modeling methamphetamine dependence and discusses possible mechanisms of methamphetamine-induced neurotoxicity. Thirdly, it provides a critical review of functional and structural neuroimaging studies in human MA abusers; including positron emission tomography (PET) and functional and structural magnetic resonance imaging (MRI). The effect of abstinence from methamphetamine, both short- and long-term within the context of these studies is also reviewed.

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Section: Dopaminergic Transmission and Glucose Metabolism Changes supporting

confidence: 82%

Functional and Structural Brain Changes Associated with Methamphetamine Abuse

2012

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“…However, in contrast to this earlier study of rat, reduced basal DA EC was apparent in our male mice only in protracted withdrawal and was paralleled by reduced DAT expression, but no discernable change in DAT function (as assessed by either Ed or the DA response to GBR-12909 infusion) (Table 4). Reduced striatal DAT binding is observed consistently in imaging studies of human MA addicts and MA-experienced non-human primates, even during protracted withdrawal (e.g., McCann et al, 1998; Sekine et al, 2001, 2003; Volkow et al, 2001a,b; Johanson et al, 2006; Groman et al, 2012). However, in MA-injected rats, reduced NAC basal DA EC was reported to co-occur with increased DAT function and expression (Broom and Yamamoto, 2005).…”

Section: Discussionmentioning

confidence: 89%

Mesocorticolimbic monoamine correlates of methamphetamine sensitization and motivation

Lominac

McKenna

Schwartz

et al. 2014

Front. Syst. Neurosci.

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Methamphetamine (MA) is a highly addictive psychomotor stimulant, with life-time prevalence rates of abuse ranging from 5–10% world-wide. Yet, a paucity of research exists regarding MA addiction vulnerability/resiliency and neurobiological mediators of the transition to addiction that might occur upon repeated low-dose MA exposure, more characteristic of early drug use. As stimulant-elicited neuroplasticity within dopamine neurons innervating the nucleus accumbens (NAC) and prefrontal cortex (PFC) is theorized as central for addiction-related behavioral anomalies, we used a multi-disciplinary research approach in mice to examine the interactions between sub-toxic MA dosing, motivation for MA and mesocorticolimbic monoamines. Biochemical studies of C57BL/6J (B6) mice revealed short- (1 day), as well as longer-term (21 days), changes in extracellular dopamine, DAT and/or D2 receptors during withdrawal from 10, once daily, 2 mg/kg MA injections. Follow-up biochemical studies conducted in mice selectively bred for high vs. low MA drinking (respectively, MAHDR vs. MALDR mice), provided novel support for anomalies in mesocorticolimbic dopamine as a correlate of genetic vulnerability to high MA intake. Finally, neuropharmacological targeting of NAC dopamine in MA-treated B6 mice demonstrated a bi-directional regulation of MA-induced place-conditioning. These results extend extant literature for MA neurotoxicity by demonstrating that even subchronic exposure to relatively low MA doses are sufficient to elicit relatively long-lasting changes in mesocorticolimbic dopamine and that drug-induced or idiopathic anomalies in mesocorticolimbic dopamine may underpin vulnerability/resiliency to MA addiction.

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“…DA is integral to the mechanism of action of Meth in adults (Hyman et al 2006) and is the major neurotransmitter affected by neurotoxic Meth exposure (O’Callaghan & Miller, 2002; Wilson et al 1996). Clinical and preclinical data have shown that adult Meth exposure can induce long-lasting decreases in levels of the DA transporter (Fleckenstein et al 1997; Johanson et al 2006; Kokoshka et al 1998; McCann et al 1998; Sekine et al 2001; Volkow et al 2001 b ; Wilson et al 1996), the vesicular monoamine transporter and DA (Friedman et al 1998; Ricaurte et al 1980; Wagner et al 1979, 1980; Wilson et al 1996). …”

Section: Discussionmentioning

confidence: 99%

Neonatal (+)-methamphetamine exposure in rats alters adult locomotor responses to dopamine D1 and D2 agonists and to a glutamate NMDA receptor antagonist, but not to serotonin agonists

Graham

Amos‐Kroohs

Braun

et al. 2012

International Journal of Neuropsychopharmacology

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AbstractNeonatal exposure to (+)-methamphetamine (Meth) results in long-term behavioural abnormalities but its developmental mechanisms are unknown. In a series of experiments, rats were treated from post-natal days (PD) 11–20 (stage that approximates human development from the second to third trimester) with Meth or saline and assessed using locomotor activity as the readout following pharmacological challenge doses with dopamine, serotonin and glutamate agonists or antagonists during adulthood. Exposure to Meth early in life resulted in an exaggerated adult locomotor hyperactivity response to the dopamine D1 agonist SKF-82958 at multiple doses, a high dose only under-response activating effect of the D2 agonist quinpirole, and an exaggerated under-response to the activating effect of the N-methyl-d-aspartic acid (NMDA) receptor antagonist, MK-801. No change in locomotor response was seen following challenge with the 5-HT releaser p-chloroamphetamine or the 5-HT2/3 receptor agonist, quipazine. These are the first data to show that PD 11-20 Meth exposure induces long-lasting alterations to dopamine D1, D2 and glutamate NMDA receptor function and may suggest how developmental Meth exposure leads to many of its long-term adverse effects.

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Cognitive function and nigrostriatal markers in abstinent methamphetamine abusers

Cited by 207 publications

References 41 publications

Functional and Structural Brain Changes Associated with Methamphetamine Abuse

Functional and Structural Brain Changes Associated with Methamphetamine Abuse

Mesocorticolimbic monoamine correlates of methamphetamine sensitization and motivation

Neonatal (+)-methamphetamine exposure in rats alters adult locomotor responses to dopamine D1 and D2 agonists and to a glutamate NMDA receptor antagonist, but not to serotonin agonists

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