Neuroscience
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Stroke is the second leading cause of death worldwide. Brain imaging data from experimental rodent stroke models suggest that size and location of the ischemic lesion relate to behavioral outcome. However, such a relationship between these two variables has not been established in Non-Human Primate (NHP) models. ⋯ The longitudinal lesion volume evaluation showed a positive correlation with the NHPSS score, whereas the remaining brain volume negatively correlated with the NHPSS. Following ROI parcellation, NHPSS outcome correlated with frontal, temporal, occipital, and middle white matter, as well as the internal capsule, and the superior temporal and middle temporal gyri, and the caudate nucleus. These results represent an important step in stroke translational research by demonstrating close similarities between the NHP stroke model and the clinical characteristics following a human stroke and illustrating significant areas that could represent targets for novel neuroprotective strategies.
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Allopregnanolone is a neurosteroid implicated in mood disorders such as depression and anxiety. It acts as a GABAA receptor (GABAAR)-positive allosteric modulator and changes the expression of GABAAR subunits and of brain-derived neurotrophic factor (BDNF) in different brain regions. It has been demonstrated that such neurochemical changes may have an asymmetrical pattern regarding brain hemispheres. ⋯ Overall hippocampal BDNF expression was also higher in the right hemisphere, but this asymmetry was not normalized by allopregnanolone. No asymmetries or changes were observed in the hippocampal mRNA expression of GABAAR subunits. These results point to a hemisphere-dependent regulation of GABAAR subunits and BDNF that can be modulated by intra-PFC allopregnanolone infusion, even in the absence of associated behavioral effects.
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This study aimed to investigate the cortical functional alterations in patients with unilateral facial synkinesis using the task-designed functional magnetic resonance imaging. Fourteen unilateral synkinesis followed by peripheral facial nerve palsy patients and eighteen healthy adults were recruited in this study. Four facial motor tasks, i.e. left/right blinking and left/right smiling, were performed by each subject during the scans. ⋯ Patients with unilateral facial synkinesis showed decreased B-S-distances during blinking and smiling tasks on the affected half face (9.68 ± 3.92 mm) compared to both average distances in healthy controls (14.95 ± 5.55 mm; p = 0.002) and unaffected half face tasks in patients (16.19 ± 7.87 mm; p = 0.011). These findings demonstrated cortical reorganization in facial synkinesis and suggested a conceivable mechanism corresponding to the simultaneous facial movement. This potentially provides a new modulation target for preventive, therapeutic and rehabilitative maneuver of this disease.
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People with Rett Syndrome (RTT), a neurodevelopmental disorder caused by mutations in the MECP2 gene, have breathing abnormalities manifested as periodical hypoventilation with compensatory hyperventilation, which are attributable to a high incidence of sudden death. Similar breathing abnormalities have been found in animal models with Mecp2 disruptions. Although RTT-type hypoventilation is believed to be due to depressed central inspiratory activity, whether this is true remains unknown. ⋯ The proportion of post-inspiratory neurons was reduced in the Mecp2-null rats. With the increased firing activity of both inspiratory and expiratory neurons in null rats, phrenic discharges shifted to a slow and deep breathing pattern. Thus, the RTT-type hypoventilation appears to result from reshaping of firing activity of both inspiratory and expiratory neurons without evident depression in central inspiratory activity.
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There is growing evidence that long noncoding RNAs (lncRNAs) play important roles in various biological processes. Metastasis-associated lung adenocarcinoma transcript 1 (MALAT1) is one of the most highly upregulated lncRNAs in cerebral ischemia. However, the molecular mechanism of MALAT1 during cerebral ischemia is still unclear. ⋯ We further revealed that MALAT1 downregulated the expression of miR-200c-3p by directly binding to miR-200c-3p. Furthermore, miR-200c-3p inhibited the autophagy and survival in BMECs by binding to 3'UTR of SIRT1, whereas MALAT1 overturned the inhibitory effect of miR-200c-3p. In conclusion, our study illuminated a novel Malat1-miR-200c-3p-SIRT1 pathway in the regulation of autophagy, in which, MALAT1 activates autophagy and promotes cell survival by binding to miR-200c-3p and upregulating SIRT1 expression.