Lithium and valproate modulate energy metabolism in an animal model of mania induced by methamphetamine

Feier, Gustavo; Valvassori, Samira S.; Varela, Roger B.; Resende, Wilson R.; Bavaresco, Daniela V.; Morais, Meline O. S.; Scaini, Giselli; Andersen, Mônica Levy; Streck, Emílio L.; Quevedo, Joao L De

doi:10.1016/j.pbb.2012.09.010

Cited by 56 publications

(35 citation statements)

References 52 publications

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“…Perhaps in recent-onset BD, compensatory mechanisms prevent the alteration of mitochondrial TCA cycle enzymes, which would be in line with the minimal changes in mitochondrial DNA content [26], mitochondrial electron transport chain activity [27], and oxidative stress [4] found in the same sample by our group. However, it is also possible that the alterations in the TCA cycle enzymes would be present only in manic phases but not in the depressive phases has suggested by abnormalities found in TCA cycle enzymes in animal models of [28] mania [10]. Another possibility would be that only later in the illness changes in the TCA cycle enzymes would take place, which is consistent with the staging model of the illness [4, 13].…”

Section: Discussionsupporting

confidence: 57%

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Regulation of leukocyte tricarboxylic acid cycle in drug-naïve Bipolar Disorder

Sousa

Streck

Forlenza

et al. 2015

Neuroscience Letters

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Several lines of evidence suggest a role for mitochondrial dysfunction in the pathophysiology of bipolar disorder (BD). The tricarboxylic acid cycle (TCA cycle) is fundamental for mitochondrial energy production and produces substrates used in oxidative phosphorylation by the mitochondrial electron transport chain. The activity of the key TCA cycle enzymes citrate synthase, malate dehydrogenase, and succinate dehydrogenase has never been evaluated in BD. In the present study, these enzymes were assayed from leukocytes of drug-naïve BD patients in a major depressive episode (n = 18) and compared to 24 age-matched healthy controls. Drug-naïve BD patients did not show differences in activities of citrate synthase (p = 0.79), malate dehydrogenase (p = 0.17), and succinate dehydrogenase (p = 0.35) compared with healthy controls. No correlation between any TCA cycle enzyme activity and severity of depressive symptoms was observed. Overall, these data suggest that the activities of the TCA cycle enzymes are not altered in major depressive episodes of recent-onset BD, which may support the concept of illness staging and neuroprogression in BD.

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Section: Discussionsupporting

confidence: 57%

“…Decreases of TCA cycle enzymes activity was observed in animal models of mania [10,11]. Moreover, BD patients have shown reduced mRNA expression of the TCA cycle enzyme malate dehydrogenase in a study evaluating postmortem brains [12].…”

Section: Introductionmentioning

confidence: 99%

Regulation of leukocyte tricarboxylic acid cycle in drug-naïve Bipolar Disorder

Sousa

Streck

Forlenza

et al. 2015

Neuroscience Letters

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“…Previous studies have shown that SD increases Per1 gene expression in several brain regions ,,. Moreover, methamphetamine a psychostimulant that induces mania‐like behavior in rats has also been shown to increase mPer1 in caudate putamen and cortex, suggesting an important role of Per1 gene in mania‐like behavior. Furthermore, we found that lithium treatment rescued Clock and Per1 gene expression to normal levels in the hippocampus and blood.…”

Section: Discussionmentioning

confidence: 90%

Lithium acts to modulate abnormalities at behavioral, cellular, and molecular levels in sleep deprivation‐induced mania‐like behavior

Andrabi

Kunjunni

et al. 2019

Bipolar Disorders

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Background: Ample amount of data suggests role of rapid eye movement (REM) sleep deprivation as the cause and effect of mania. Studies have also suggested disrupted circadian rhythms contributing to the pathophysiology of mood disorders, including bipolar disorder. However, studies pertaining to circadian genes and effect of lithium treatment on clock genes are scant. Thus, we wanted to determine the effects of REM sleep deprivation on expression of core clock genes and determine whether epigenetics is involved. Next, we wanted to explore ultrastructural abnormalities in the hippocampus. Moreover, we were interested to determine oxidative stress, tumor necrosis factor-α (TNF-α), and brain-derived neurotrophic factor levels in the central and peripheral systems.Methods: Rats were sleep deprived by the flower pot method and were then analyzed for various behaviors and biochemical tests. Lithium was supplemented in diet. Results:We found that REM sleep deprivation resulted in hyperactivity, reduction in anxiety-like behavior, and abnormal dyadic social interaction. Some of these behaviors were sensitive to lithium. REM sleep deprivation also altered circadian gene expression and caused significant imbalance between histone acetyl transferase/ histone deacetylase (HAT/HDAC) activity. Ultrastructural analysis revealed various cellular abnormalities. Lipid peroxidation and increased TNF-α levels suggested oxidative stress and ongoing inflammation. Circadian clock genes were differentially modulated with lithium treatment and HAT/HDAC imbalance was partially prevented.Moreover, lithium treatment prevented myelin fragmentation, disrupted vasculature, necrosis, inflammation, and lipid peroxidation, and partially prevented mitochondrial damage and apoptosis. Conclusions:Taken together, these results suggest plethora of abnormalities in the brain following REM sleep deprivation, many of these changes in the brain may be target of lithium's mechanism of action. K E Y W O R D SBDNF, circadian clock, HAT/HDAC, mania, oxidative stress, REM sleep deprivation | 267 ANDRABI et Al

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“…Valvassori et al 90 showed that AMPH inhibited mitochondrial respiratory chain activity in rat brains, and VPA, but not Li, reversed this. Feier et al 91 showed that methamphetamine inhibited the activities of Krebs cycle enzymes and complexes of the mitochondrial respiratory chain, and Li and VPA reversed methamphetamine-induced energy metabolism dysfunction.…”

Section: Bipolar Disordermentioning

confidence: 99%

Mitochondria and the central nervous system: searching for a pathophysiological basis of psychiatric disorders

Streck

Gonçalves

Furlanetto

et al. 2014

Rev. Bras. Psiquiatr.

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Introduction: Mitochondrial dysfunction has been postulated to participate in the development of many neuropsychiatric disorders, but there is no consensus as to its role. The aim of this paper is to review recent studies and to outline the current understanding of the association between mitochondrial dysfunction and psychiatric disorders. Methodology: We reviewed articles that evaluated mitochondrial dysfunction and psychiatric disorders, with a particular focus on depression, bipolar disorder, anxiety disorders, obsessivecompulsive disorder, and autism spectrum disorder, and the association between mitochondrial dysfunction and development of these disorders. Results: Evidence suggests that alterations in mitochondrial morphology, brain energy metabolism, and mitochondrial enzyme activity may be involved in the pathophysiology of different neuropsychiatric disorders, given their key role in energy metabolism in the cell. Conclusions: Understanding the interactions between mitochondrial dysfunction and development of psychiatric disorders may help establish more effective therapeutic strategies for these disorders and thus lead to better outcomes for affected subjects.

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Lithium and valproate modulate energy metabolism in an animal model of mania induced by methamphetamine

Cited by 56 publications

References 52 publications

Regulation of leukocyte tricarboxylic acid cycle in drug-naïve Bipolar Disorder

Regulation of leukocyte tricarboxylic acid cycle in drug-naïve Bipolar Disorder

Lithium acts to modulate abnormalities at behavioral, cellular, and molecular levels in sleep deprivation‐induced mania‐like behavior

Mitochondria and the central nervous system: searching for a pathophysiological basis of psychiatric disorders

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