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• W2182269063 endingPage "385" @default.
• W2182269063 startingPage "375" @default.
• W2182269063 abstract "Schizophrenia, a major psychiatric disease, affects individuals in the centre of their personality. Its aetiology is not clearly established. In this review, we will present evidence that patients suffering of schizophrenia present a brain deficit in glutathione, a major endogenous redox regulator and antioxidant. We will also show that, in experimental models, a decrease in glutathione, particularly during development, induces morphological, electrophysiological and behavioural anomalies consistent with those observed in the disease. In the cerebrospinal fluid of drug-naive schizophrenics, glutathione level was decreased by 27% and its direct metabolite of glutathione by 16%. Glutathione level in prefrontal cortex of patients, measured by magnetic resonance spectroscopy, was 52% lower than in controls. Patients’ fibroblasts reveal a decrease in mRNA levels of the two glutathione synthesising enzymes, glutamatecysteine ligase modulatory subunit (GCLM) and glutathione synthetase. GCLM expression level in fibroblasts correlates negatively with symptoms severity. Glutathione is an important endogenous redox regulator and neuroactive substance. It is protecting cells from damage by reactive oxygen species generated, among others, by dopamine metabolism.A glutathione deficit-induced oxidative stress would lead to lipid peroxidation and micro-lesions at the level of dendritic spines, a synaptic damage responsible for abnormal nervous connections or structural disconnectivity. On the other hand, a glutathione deficit could also lead to a functional disconnectivity by depressing NMDA neurotransmission, in analogy to phencyclidine effects. Present experimental data are consistent with the proposed hypothesis: decreasing pharmacologically glutathione level in experimental models, with or without blocking dopamine (DA) uptake (GBR12909), induces morphological, electrophysiological and behavioural changes similar to those observed in patients: ‐ Dendritic spines and GABA interneurons: (a) In neuronal cultures, low glutathione level and dopamine induce decreased density of neural processes; (b) in developing rats (p5‐p16), glutathione-level deficit and GBR induce a decrease in normal spines in prefrontal pyramids and in GABA-parvalbumin but not in -calretinin immunoreactivity in anterior cingulated cortex. ‐ NMDA-dependent synaptic plasticity: Glutathione depletion impairs NMDA responses in neuronal cultures and long-term potentiation in hippocampal slices. ‐ Cognition:Developing rats with low glutathione level and GBR have deficits in olfactory integration and object recognition, deficit which appears earlier in males than females, in analogy to the delay of the psychosis onset between man and woman." @default.
• W2182269063 created "2016-06-24" @default.
• W2182269063 creator A5076937097 @default.
• W2182269063 creator A5078640014 @default.
• W2182269063 creator A5078914193 @default.
• W2182269063 date "2004-12-01" @default.
• W2182269063 modified "2023-10-17" @default.
• W2182269063 title "Schizophrenia: glutathione deficit as a new vulnerability factor for disconnectivity syndrome" @default.
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