Decreased Creatine Kinase Activity Caused by Electroconvulsive Shock

Búrigo, Márcio; Roza, Clarissa A.; Bassani, Cintia; Dal‐Pizzol, Felipe; Quevedo, Joao L De; Streck, Emílio L.

doi:10.1007/s11064-006-9091-1

Cited by 19 publications

(17 citation statements)

References 36 publications

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“…The effect of electroconvulsive shock (an animal model for electroconvulsive therapy) showed increased activities of mitochondrial respiratory chain complexes II and IV [64], and inhibition on creatine kinase activity in brain of rats [65].…”

Section: Depressionmentioning

confidence: 99%

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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Section: Depressionmentioning

confidence: 99%

Mitochondrial Dysfunction and Psychiatric Disorders

et al. 2008

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“…Some studies showed that reductions of regional cerebral blood flow or regional cerebral metabolic rate occur after ECT, especially in cerebral cortex, suggesting a possible suppression of brain activity [20], associated with better clinical outcome [21]. In this context, we have recently shown that acute and chronic ECS decreased creatine kinase activity in brain of rats [22].…”

Section: Discussionmentioning

confidence: 91%

Effect of Electroconvulsive Shock on Mitochondrial Respiratory Chain in Rat Brain

et al. 2006

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It is well described that impairment of energy production has been implicated in the pathogenesis of a number of diseases. Although several advances have occurred over the past 20 years concerning the use and administration of electroconvulsive therapy (ECT) to minimize its side effects, little progress has been made in understanding its mechanism of action. In this work, our aim was to measure the activities of mitochondrial respiratory chain complexes II and IV and succinate dehydrogenase from rat brain after acute and chronic electroconvulsive shock (ECS). Our results showed that mitochondrial respiratory chain enzymes activities were increased after acute ECS in hippocampus, striatum and cortex of rats. Besides, we also demonstrated that complex II activity was increased after chronic ECS in cortex, while hippocampus and striatum were not affected. Succinate dehydrogenase, however, was inhibited after chronic ECS in striatum, activated in cortex and not affected in hippocampus. Finally, complex IV was not affected by chronic ECS in hippocampus, striatum and cortex. Our findings demonstrated that brain metabolism is altered by ECS.

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“…Different groups of rats (n = 8 each 33,34 ) were administered intraperitoneally with saline or different doses of ketamine (5, 10 and 15mg/kg) or imipramine (10, 20 and 30mg/kg) 60 minutes before the test session (forced swimming test). The range of doses of ketamine employed in this work was chosen based on a previous study, which reported an increase in spontaneous locomotor activity at 25mg/kg, while no changes were observed at 10mg/kg.…”

Section: Acute Administration Of Ketamine and Imipraminementioning

confidence: 99%

“…[27][28][29][30][31] We have recently showed that brain CK activity is inhibited by antipsychotics (haloperidol and olanzapine), 32 in animal models of neuropsychiatry disorders, such as bipolar disorder 33 and after electroconvulsive shock. 34 Brain and other high-energy consuming tissues are more susceptible to reduction of energy metabolism. Neuropsychiatry disorders, such as schizophrenia, depression and bipolar disorder have been related to dysfunction in brain metabolism.…”

Section: Introductionmentioning

confidence: 99%