Behavioural brain research
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Transcranial magnetic stimulation is an established method to probe inhibitory and facilitatory networks within the human motor cortex. Reduced motor-cortical inhibition is a common finding in schizophrenia patients. Based on neuropathological findings, the reduced cortical inhibition in schizophrenia has been linked mainly to alterations in GABAergic neurotransmission. ⋯ An overall comparison between HC and all patients showed a significantly reduced SICI (p=0.031) and prolonged CSP (p=0.003) in schizophrenia patients. This is the largest and first cross-sectional investigation of various excitability parameters in schizophrenia patients. These findings indicate general alterations of cortical inhibition, with differences between recent-onset and chronically-ill schizophrenia patients.
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Depression is one of the most common neuropsychiatric disorders and has been associated with the neuroendocrine system and alterations in specific brain proteins. Resveratrol is a natural polyphenol enriched in polygonum cuspidatum and has diverse biological activities, including potent antidepressant-like effects. The present study attempts to explore the mechanisms underlying the antidepressant-like action of resveratrol by measuring serum corticosterone levels and the content of brain derived neurotrophic factor (BDNF) in the hippocampus and amygdala of rats exposed to the chronic unpredictable mild stress (CUMS). ⋯ Additionally, 5-weeks of CUMS exposure significantly decreased BDNF levels in the hippocampus and amygdala, and was accompanied by decreased phosphorylation of extracellular signal-regulated kinase (pERK) and cAMP response element-binding protein (pCREB), while resveratrol treatment normalized these levels. All of these effects of resveratrol were essentially identical to that observed with the established antidepressant, desipramine. In conclusion, our study shows that resveratrol exerted antidepressant-like effects in CUMS rats, mediated in part by normalizing serum corticosterone levels while up-regulating pERK, pCREB and BDNF levels in the hippocampus and amygdala.
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Defect of autophagy is common to many neurodegenerative disorders because it serves as a major degradation pathway for the clearance of various aggregate-prone proteins. Mammalian target of rapamycin (mTOR) signaling, which is recognized as the most important negative regulator of autophagy, is also involved in neurodegenerative diseases. However, the role of mTOR and its dependent autophagy in normal brain during aging remains unknown. ⋯ However, whether CR can ameliorate age-related cognition deficits by inhibiting mTOR and activate autophagy in hippocampus needs to be further investigated. Here we showed a decline of autophagic degradation in mice hippocampus in correlation with age-dependent cognitive dysfunction, whereas the activity of mTOR and its upstream brain-derived neurotrophic factor (BDNF)/phosphatidylinositide 3-kinase (PI3K)/protein kinase B (Akt) signaling was decreased with aging. In addition, facilitating the mTOR pathway successfully declines and sustains autophagic degradation with aging in hippocampus by CR treatment and is involved in CR by ameliorating age-related cognitive deficits.