Lithium and valproate attenuate dextroamphetamine-induced changes in brain activation

Bell, Emily C.; Willson, Morgan C.; Wilman, Alan H.; Dave, Sanjay; Asghar, Sheila; Silverstone, Peter H.

doi:10.1002/hup.665

Cited by 35 publications

(20 citation statements)

References 49 publications

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“…Both treatment groups had a significant decrease in BOLD signal during the word generation paradigm after treatment, compared with the placebo group. Previously our research group has shown that lithium and valproate exert task and region dependent effects on dextroamphetamine-induced changes in brain activation (Bell et al, 2005). The current study demonstrates that lithium and valproate, alone, exert differential effects on brain activity in healthy control subjects.…”

Section: Discussionmentioning

confidence: 55%

Differential effects of chronic lithium and valproate on brain activation in healthy volunteers

Bell

Willson

Wilman

et al. 2005

Hum. Psychopharmacol. Clin. Exp.

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Section: Discussionmentioning

confidence: 55%

Differential effects of chronic lithium and valproate on brain activation in healthy volunteers

Bell

Willson

Wilman

et al. 2005

Hum. Psychopharmacol. Clin. Exp.

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“…According to this study, the inhibition of activity of citrate synthase may be probably related to the pathophysiology of this disease [36]. There are some studies showing that amphetamine induces changes in various systems, such as signaling pathways and kinases and phosphatases activities, and that mood stabilizers prevent and/or reverse some of these biochemical and other behavioral effects caused by amphetamine [37][38][39][40][41].…”

Section: Bipolar Disordermentioning

confidence: 84%

Mitochondrial Dysfunction and Psychiatric Disorders

et al. 2008

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Mitochondrial oxidative phosphorylation is the major ATP-producing pathway, which supplies more than 95% of the total energy requirement in the cells. Damage to the mitochondrial electron transport chain has been suggested to be an important factor in the pathogenesis of a range of psychiatric disorders. Tissues with high energy demands, such as the brain, contain a large number of mitochondria, being therefore more susceptible to reduction of the aerobic metabolism. Mitochondrial dysfunction results from alterations in biochemical cascade and the damage to the mitochondrial electron transport chain has been suggested to be an important factor in the pathogenesis of a range of neuropsychiatric disorders, such as bipolar disorder, depression and schizophrenia. Bipolar disorder is a prevalent psychiatric disorder characterized by alternating episodes of mania and depression. Recent studies have demonstrated that important enzymes involved in brain energy are altered in bipolar disorder patients and after amphetamine administration, an animal model of mania. Depressive disorders, including major depression, are serious and disabling. However, the exact pathophysiology of depression is not clearly understood. Several works have demonstrated that metabolism is impaired in some animal models of depression, induced by chronic stress, especially the activities of the complexes of mitochondrial respiratory chain. Schizophrenia is a devastating mental disorder characterized by disturbed thoughts and perception, alongside cognitive and emotional decline associated with a severe reduction in occupational and social functioning, and in coping abilities. Alterations of mitochondrial oxidative phosphorylation in schizophrenia have been reported in several brain regions and also in platelets. Abnormal mitochondrial morphology, size and density have all been reported in the brains of schizophrenic individuals. Considering that several studies link energy impairment to neuronal death, neurodegeneration and disease, this review article discusses energy impairment as a mechanism underlying the pathophysiology of some psychiatric disorders, like bipolar disorder, depression and schizophrenia.

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“…Despite of the well-recognized limitations of animal models of bipolar disorder in terms of face validity (Machado-Vieira et al, 2004;Einat et al, 2000), it is well known that AMPH induces manic symptoms in BD patients (Anand et al, 2000) as well as in healthy volunteers (Strakowski and Sax, 1998). Using fMRI, Bell et al (2005) reported that Li and VPT attenuated AMPH-induced changes in human brain during neuropsychological tasks. In addition, Beaulieu et al (2004) recently found that the hyperactivity induced by AMPH is partially mediated by Akt/glycogen synthase kinase-3β (GSK-3β) signaling pathway and that Li was able to reverse this effect.…”

Section: Discussionmentioning

confidence: 98%

Effects of mood stabilizers on hippocampus BDNF levels in an animal model of mania

et al. 2006

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Lithium and valproate attenuate dextroamphetamine-induced changes in brain activation

Cited by 35 publications

References 49 publications

Differential effects of chronic lithium and valproate on brain activation in healthy volunteers

Differential effects of chronic lithium and valproate on brain activation in healthy volunteers

Mitochondrial Dysfunction and Psychiatric Disorders

Effects of mood stabilizers on hippocampus BDNF levels in an animal model of mania

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