Brain creatine kinase activity in an animal model of mania

Streck, Emílio L.; Amboni, Graziela; Scaini, Giselli; Di-Pietro, Priscila B.; Rezin, Gislaine T.; Valvassori, Samira S.; Luz, Gabrielle da; Kapczinski, Flávio; Quevedo, João

doi:10.1016/j.lfs.2007.11.026

Cited by 52 publications

(36 citation statements)

References 48 publications

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“…12,14,15 Furthermore, there is strong evidence that metabolic impairment and mitochondrial dysfunction are involved in the pathophysiology of BD. [16][17][18][19][20] The phosphocreatine/ CK energy circuit, which is important for maintaining normal energy homeostasis, 21,22 has a number of integrated functions, such as temporary energy buffering and energy transfer, as well as regulating metabolic capacity. 23 In view of these data, we can suggest that the increased CK activity seen in manic BD patients is a compensatory mechanism related to the mitochondrial damage that occurs in BD.…”

Section: Discussionmentioning

confidence: 99%

“…In addition, decreased CK activity has been reported in a rat model of d-amphetamine-induced mania. 20 That finding could be explained by the fact that increased dopamine activity inhibits CK. In a clinical study of patients with bipolar I or II disorder (BP I or BP II), 26 brain phosphorus metabolism was measured by phosphorus-31 magnetic resonance spectroscopy.…”

Section: Discussionmentioning

confidence: 99%

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Creatine kinase levels in patients with bipolar disorder: depressive, manic, and euthymic phases

Valvassori

Rezin

Búrigo

et al. 2011

Rev. Bras. Psiquiatr.

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Objective: Bipolar disorder is a severe, recurrent, and often chronic psychiatric illness associated with significant functional impairment, morbidity, and mortality. Creatine kinase is an important enzyme, particularly for cells with high and fluctuating energy requirements, such as neurons, and is a potential marker of brain injury. The aim of the present study was to compare serum creatine kinase levels between bipolar disorder patients, in the various phases (depressive, manic, and euthymic), and healthy volunteers. Method: Forty-eight bipolar patients were recruited: 18 in the euthymic phase; 17 in the manic phase; and 13 in the depressive phase. The control group comprised 41 healthy volunteers. The phases of bipolar disorder were defined as follows: euthymic-not meeting the DSM-IV criteria for a mood episode and scoring < 8 on the Hamilton Depression Rating Scale (HDRS) and Young Mania Rating Scale (YMRS); manic-scoring < 7 on the HDRS and > 7 on the YMRS; depressive-scoring > 7 on the HDRS and < 7 on the YMRS. Patients in mixed phases were excluded. Blood samples were collected from all participants. Results: Creatine kinase levels were higher in the manic patients than in the controls. However, we observed no significant difference between euthymic and depressive patients in terms of the creatine kinase level. Conclusion: Our results suggest that the clinical differences among the depressive, manic, and euthymic phases of bipolar disorder are paralleled by contrasting levels of creatine kinase. However, further studies are needed in order to understand the state-dependent differences observed in serum creatine kinase activity. Descriptors

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Creatine kinase levels in patients with bipolar disorder: depressive, manic, and euthymic phases

Valvassori

Rezin

Búrigo

et al. 2011

Rev. Bras. Psiquiatr.

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“…[84][85][86] Corrê a et al 87 showed that citrate synthase activity was inhibited in the rat hippocampus after mania induced by amphetamine, and this was reversed by valproate (VPA) and lithium (Li) administration. In contrast, Streck et al 88 demonstrated that amphetamine inhibited creatine kinase activity in rat brains, but VPA and Li were not able to prevent this. Zugno et al 89 showed that amphetamine increased Na + , K + -ATPase activity in rat brains, and that VPA or Li reversed this effect.…”

Section: Bipolar Disordermentioning

confidence: 89%

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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“…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%

“…[24][25][26] It is also known that a decrease in Creatine kinase activity may potentially impair energy homeostasis, contributing to cell death. [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.…”

Section: Introductionmentioning

confidence: 99%

Effect of acute administration of ketamine and imipramine on creatine kinase activity in the brain of rats

Assis

Rezin

Comim

et al. 2009

Rev. Bras. Psiquiatr.

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Brain creatine kinase activity in an animal model of mania

Cited by 52 publications

References 48 publications

Creatine kinase levels in patients with bipolar disorder: depressive, manic, and euthymic phases

Creatine kinase levels in patients with bipolar disorder: depressive, manic, and euthymic phases

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

Effect of acute administration of ketamine and imipramine on creatine kinase activity in the brain of rats

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