Normalization of cytochrome-c oxidase activity in the rat brain by neuroleptics after chronic treatment with PCP or methamphetamine
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Cited by (31)
Parkin-deficient rats are resistant to neurotoxicity of chronic high-dose methamphetamine
2021, Experimental NeurologyCitation Excerpt :Interestingly, chronic self-administration of ~1.5 mg/kg/d METH lead to decreased levels of some complex I subunits (NDUFS1, NDUFV1) and increases in others (NUFS5) within rats striatal synaptosomes at 14 days after the last operant session; no changes in complex II subunits were detected (Bosch et al., 2015). Price and colleagues observed no change in complex II activity and decreased complex IV activity in the striatum after 28 days of chronic treatment with 5 mg/kg METH (Prince et al., 1997). The data suggests that changes in the levels of ETC enzyme subunits are time-, species-, and METH-dose dependent.
Mitochondrial impairment, apoptosis and autophagy in a rat brain as immediate and long-term effects of perinatal phencyclidine treatment - influence of restraint stress
2016, Progress in Neuro-Psychopharmacology and Biological PsychiatryCitation Excerpt :Deficits in mitochondrial respiratory chain complexes (Maurer et al., 2001) and reduced numbers and volume of mitochondria have been identified in the cortex and other brain regions of schizophrenia patients (Kung and Roberts, 1999; Uranova et al., 2001). There is accumulating evidence that a reduction of COX activity in the frontal cortex contributes to schizophrenia pathogenesis (Prince et al., 1997a,b). A reduction of COX activity was observed in the frontal cortex and caudate nuclei in schizophrenic vs. control brain tissue (Cavelier et al., 1995).
Schizophrenia: Maternal inheritance and heteroplasmy of mtDNA mutations
2012, Molecular Genetics and MetabolismCitation Excerpt :Methamphetamine, which induces psychosis in normal individuals, reduced COX activity and conversely, treatment with neuroleptic agents such as clozapine and fluphenazine increased this enzyme activity in the frontal cortex of rat brains. Moreover, the methamphetamine-induced reduction of COX activity is prevented by the use of neuroleptic agents [14, 15]. Furthermore, there is a relationship between the accumulation of mtDNA deletions in an individual cell and a reduction of COX activity, and these deletions increase with aging in normal individuals [16].
Mitochondrial dysfunction and pathology in bipolar disorder and schizophrenia
2011, International Journal of Developmental NeuroscienceCitation Excerpt :For example, SZ patients showed large reductions in cytochrome-c oxidase activity in the caudate nucleus, the frontal cortex and the temporal cortex (Cavelier et al., 1995; Maurer et al., 2001). Rodent studies suggest that this reduction is not caused by treatment (Prince et al., 1997a,b). In the PFC of BPD patients, complex I activity was impaired and associated with increased protein oxidation and nitration (Andreazza et al., 2010).
Changes in brain oxidative metabolism induced by inhibitory avoidance learning and acute administration of amitriptyline
2008, Pharmacology Biochemistry and Behavior