Mitochondrial dysfunction in schizophrenia: a possible linkage to dopamine

Mitochondria are not only the principal source of high energy intermediates, but play an important role in intracellular calcium buffering, are main producers of reactive oxygen species, and are the source of pro‐ and antiapoptotic key factors. Moreover, the mitochondria are of a ubiquitous nature a...

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Bibliographic Details
Published in:Journal of neurochemistry 2002-12, Vol.83 (6), p.1241-1251
Main Author: Ben‐Shachar, Dorit
Format: Article
Language:English
Subjects:
Adult and adolescent clinical studies
Animals
Antipsychotic Agents - pharmacology
Biological and medical sciences
Brain - physiopathology
cytochrome c oxidase
dopamine
Dopamine - metabolism
Electron Transport Complex I
Energy Metabolism
Gene Expression
Humans
Medical sciences
mitochondria
Mitochondria - metabolism
mitochondrial respiration chain
NADH, NADPH Oxidoreductases - antagonists & inhibitors
NADH, NADPH Oxidoreductases - metabolism
NADH‐ubiquinone oxidoreductase (complex I)
Oxidative Phosphorylation
Psychology. Psychoanalysis. Psychiatry
Psychopathology. Psychiatry
Psychoses
Schizophrenia
Schizophrenia - drug therapy
Schizophrenia - etiology
Schizophrenia - physiopathology
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Summary:Mitochondria are not only the principal source of high energy intermediates, but play an important role in intracellular calcium buffering, are main producers of reactive oxygen species, and are the source of pro‐ and antiapoptotic key factors. Moreover, the mitochondria are of a ubiquitous nature and the respiratory chain has a dual genetic basis, i.e. the mitochondrial and the nuclear DNAs. Thus mitochondrial impairment could provide an explanation for the tremendous heterogeneity of clinical and pathological manifestations in schizophrenia. This article reviews several independent lines of evidence that suggest an involvement of mitochondrial dysfunction in schizophrenia. Among them are altered cerebral energy metabolism, mitochondrial hypoplasia, dysfunction of the oxidative phosphorylation system and altered mitochondrial related gene expression. In addition, the interaction between dopamine, a predominant etiological factor in schizophrenia, and mitochondrial respiration is considered as a possible mechanism underlying the hyper‐ and hypo‐activity cycling in schizophrenia. Understanding the role of mitochondria in schizophrenia may encourage novel treatment approaches, the identification of candidate genes and new insights into the pathophysiology and etiology of the disorder.
ISSN:0022-3042
1471-4159
DOI:10.1046/j.1471-4159.2002.01263.x