Impaired Prefrontal Cortical Function and Disrupted Adaptive Cognitive Control in Methamphetamine Abusers: A Functional Magnetic Resonance Imaging Study

Salo, Ruth; Ursu, Stefan; Buonocore, Michael H.; Leamon, Martin H.; Carter, Cameron

doi:10.1016/j.biopsych.2008.11.026

Cited by 128 publications

(145 citation statements)

References 20 publications

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“…Our observation of greater activation of the ACC under modafinil than placebo conditions in the MA group has particular therapeutic relevance, as the ACC has been shown to be hypoactive in MA subjects (as compared with activity in control subjects) during tests of cognitive control (Salo et al, 2009) and vigilance . The boost in ACC activation observed with modafinil likely reflects greater engagement of cognitive processes important for learning, especially as ACC activation has been previously shown to correlate positively with learning performance on this task in control subjects (Ghahremani et al, 2010).…”

Section: Discussionmentioning

confidence: 69%

“…Moreover, MA-dependent subjects exhibit abnormal structure and function of the anterior cingulate cortex (ACC) Salo et al, 2009;Thompson et al, 2004), a cortical structure that is associated with reward processing and has a major projection to dopamine-rich ventral striatal areas (Haber and Knutson, 2010). In light of evidence that modafinil raises ACC activation from a hypoactive state in patient groups (eg, schizophrenia) commensurate with improving behavioral performance in some participants (Spence et al, 2005), ACC appears to be a likely cortical target for the potential cognition-enhancing benefits of modafinil in MA-dependent subjects.…”

Section: Introductionmentioning

confidence: 99%

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Effect of Modafinil on Learning and Task-Related Brain Activity in Methamphetamine-Dependent and Healthy Individuals

Ghahremani

Tabibnia

Monterosso

et al. 2011

Neuropsychopharmacol

108

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Methamphetamine (MA)-dependent individuals exhibit deficits in cognition and prefrontal cortical function. Therefore, medications that improve cognition in these subjects may improve the success of therapy for their addiction, especially when cognitive behavioral therapies are used. Modafinil has been shown to improve cognitive performance in neuropsychiatric patients and healthy volunteers. We therefore conducted a randomized, double-blind, placebo-controlled, cross-over study, using functional magnetic resonance imaging, to examine the effects of modafinil on learning and neural activity related to cognitive function in abstinent, MA-dependent, and healthy control participants. Modafinil (200 mg) and placebo were administered orally (one single dose each), in counterbalanced fashion, 2 h before each of two testing sessions. Under placebo conditions, MA-dependent participants showed worse learning performance than control participants. Modafinil boosted learning in MA-dependent participants, bringing them to the same performance level as control subjects; the control group did not show changes in performance with modafinil. After controlling for performance differences, MAdependent participants showed a greater effect of modafinil on brain activation in bilateral insula/ventrolateral prefrontal cortex and anterior cingulate cortices than control participants. The findings suggest that modafinil improves learning in MA-dependent participants, possibly by enhancing neural function in regions important for learning and cognitive control. These results suggest that modafinil may be a suitable pharmacological adjunct for enhancing the efficiency of cognitive-based therapies for MA dependence. Neuropsychopharmacology (2011) 36, 950-959;

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Section: Discussionmentioning

confidence: 69%

Section: Introductionmentioning

confidence: 99%

Effect of Modafinil on Learning and Task-Related Brain Activity in Methamphetamine-Dependent and Healthy Individuals

Ghahremani

Tabibnia

Monterosso

et al. 2011

Neuropsychopharmacol

108

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“…These meth-induced cortical disruptions may reduce the ability to regulate subcortical drives in limbic structures, including the NAc (Goldstein et al, 2009). Consistent with this hypothesis, human meth addicts often exhibit enduring PFC-dependent cognitive deficits in tasks requiring attention, working memory, and suppression of irrelevant information (Baicy and London, 2007;Salo et al, 2009), as well as enduring downregulation of DA transporter (DAT) function in the frontal cortex, NAc, and caudate/putamen (Chang et al, 2007;McCann et al, 2008). Reductions in basal NAc GLU following cocaine selfadministration have been attributed to decreased affinity of the cystine-GLU exchanger (Baker et al, 2003;McFarland et al, 2003).…”

Section: Discussionmentioning

confidence: 86%

“…Methamphetamine (meth) addicts often exhibit pronounced deficits in cortical regulation of subcortical drive (Baicy and London, 2007;Salo et al, 2009). The impact of meth on this circuitry may be more profound than other addictive drugs, due in part to its long half-life, high-lipid solubility, fast uptake and accumulation, and distinctive pharmacological effects on both DA and GLU functions (Bowyer et al, 2008;Fowler et al, 2008;Stephans and Yamamoto, 1994).…”

Section: Introductionmentioning

confidence: 99%

Dysregulation of Dopamine and Glutamate Release in the Prefrontal Cortex and Nucleus Accumbens Following Methamphetamine Self-Administration and During Reinstatement in Rats

Parsegian

See

2013

Neuropsychopharmacol

106

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Methamphetamine (meth) addicts often exhibit enduring cognitive and neural deficits that likely contribute to persistent drug seeking and the high rates of relapse. These deficits may be related to changes in the prefrontal cortex (PFC) and its glutamatergic projections to the nucleus accumbens (NAc). Here, we performed in vivo microdialysis in the PFC and NAc in rats following either meth self-administration or yoked-saline control histories to assess baseline glutamate (GLU) levels, or reinstatement-evoked GLU and dopamine (DA) efflux in both regions simultaneously under cue-induced, meth-primed, or combined cues þ meth reinstatement conditions. Our results show that meth self-administration (1) reduced basal GLU levels in both the dmPFC and NAc, (2) concurrently increased dmPFC and NAc GLU efflux during reinstatement, and (3) increased DA efflux in the dmPFC, but not in the NAc, under all reinstatement conditions when compared with yoked-saline controls. These data demonstrate for the first time that a history of psychostimulant self-administration alters GLU homeostasis not only in the NAc, but also in the dmPFC, its primary GLU projection source. Furthermore, combined cues þ meth-primed reinstatement conditions produced the most pronounced increases in mPFC and NAc extracellular GLU, suggesting that the cue and meth prime conditions are additive in promoting reinstatement. Finally, increased efflux of DA in the dmPFC, but not in the NAc, across reinstatement conditions suggests that DA release in the dmPFC may be an important mediator of drug seeking initiated by multiple relapse triggers. Neuropsychopharmacology (2014) 39, 811-822; doi:10.1038/npp.2013; published online 9 October 2013 Keywords: dopamine; glutamate; methamphetamine self-administration; nucleus accumbens; prefrontal cortex; reinstatement INTRODUCTIONThe development of drug addiction is believed to derive in large part from maladaptive neurobiological responses to drugs of abuse within the corticostriatal glutamate (GLU) and mesostriatal dopamine (DA) systems of the brain (Berridge and Robinson, 1998;Wise, 2004;Kalivas et al, 2005). Although these circuits normally optimize behavior in response to a changing environment and establish welllearned behaviors, their dysregulation due to repeated drug abuse likely underlies the switch to habitual drug-taking behaviors, which operate outside of normal cortical regulation (Goldstein et al, 2009;George and Koob, 2010).Methamphetamine (meth) addicts often exhibit pronounced deficits in cortical regulation of subcortical drive (Baicy and London, 2007;Salo et al, 2009). The impact of meth on this circuitry may be more profound than other addictive drugs, due in part to its long half-life, high-lipid solubility, fast uptake and accumulation, and distinctive pharmacological effects on both DA and GLU functions (Bowyer et al, 2008;Fowler et al, 2008;Stephans and Yamamoto, 1994). Thus, meth abuse may alter DA receptive pyramidal neurons in the PFC, in turn affecting downstream signaling in the nucleus accum...

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“…27 Furthermore, individuals with schizophrenia and stimulant drug addiction exhibit exaggerated striatal DA release in response to an amphetamine challenge, but appear to have blunted DA activity in the mPFC. [28][29][30][31][32][33][34][35][36] (For possible mechanisms accounting for the inhibitory control of DA activity in mPFC over DA activity in the nucleus accumbens, see Carr and Sesack, 10 Sesack and Pickel 37 and Gao and colleagues.…”

Section: Reciprocal Relations Between Mesolimbic and Mesocortical Da mentioning

confidence: 99%

Role of netrin-1 in the organization and function of the mesocorticolimbic dopamine system

Flores

2011

jpn

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Impaired Prefrontal Cortical Function and Disrupted Adaptive Cognitive Control in Methamphetamine Abusers: A Functional Magnetic Resonance Imaging Study

Cited by 128 publications

References 20 publications

Effect of Modafinil on Learning and Task-Related Brain Activity in Methamphetamine-Dependent and Healthy Individuals

Effect of Modafinil on Learning and Task-Related Brain Activity in Methamphetamine-Dependent and Healthy Individuals

Dysregulation of Dopamine and Glutamate Release in the Prefrontal Cortex and Nucleus Accumbens Following Methamphetamine Self-Administration and During Reinstatement in Rats

Role of netrin-1 in the organization and function of the mesocorticolimbic dopamine system

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