Neuroscience
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The medial olivocochlear (MOC) system is thought to be responsible for modulation of peripheral hearing through descending (efferent) pathways. This study investigates the connection between peripheral hearing function and auditory attention tasks of different degrees of difficulty. Peripheral hearing function was evaluated by analyzing the amount of change in otoacoustic emissions (OAEs) by contralateral acoustic stimulation (CAS), a well-known effect of the MOC system. ⋯ There was also no effect on OAE latency, nor was there any difference in noise level or number of rejected trials. However, we observed that the changes in OAEs by CAS for easy and hard tasks were correlated with the magnitude of the P3 wave in the ERP. This suggests there might be some sort of mutual compensation mechanism - presently unknown - between periphery and cortex.
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Stress-related mood disorders like anxiety and depression are more prevalent in women than men and are often associated with hypothalamic-pituitary-adrenal (HPA) axis dysregulation. Androgen actions through androgen receptors (ARs) decrease HPA axis responses and stress-associated behaviors. Corticotropin releasing factor (CRF) and its binding to CRF receptor 1 (CRFR1) is also critical for regulation of the HPA axis, anxiety, and depression. ⋯ Following restraint stress GDX-blank mice showed fewer c-Fos/CRFR1 co-localized neurons in the MePD compared to gonad intact and GDX-DHT groups indicating decreased stress-induced activation of CRFR1 neurons following GDX. Higher plasma corticosterone (CORT) was found in GDX males compared to GDX-DHT and sham males following restraint stress, with a negative correlation between PVN CRFR1+ neurons and corticosterone levels 30- and 90-min following restraint. Together these findings show androgens can directly alter CRFR1 levels in the brain which may have implications for sex differences in regulation of the HPA axis and stress-related behaviors.
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Although various studies have reported a high prevalence of depression among Parkinson's disease (PD) patients, the pathophysiological mechanism of depression in PD (DPD) is still unclear. The core region of the reward network, the ventral striatum (VS), is critical in the occurrence and development of DPD. This study aimed to explore the altered functional connectivity (FC) of VS subregions in DPD. ⋯ The hyperconnectivity between vCa_L and the MOG. L might be viewed as a compensatory mechanism for depression in the early stage of PD. This study provides new insight into the neural mechanism of depression in the early stage of PD and contributes to explore the potential neuroimaging markers for DPD.
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Growing evidence has demonstrated that treadmill exercise is beneficial to increase β-amyloid (Aβ) clearance and protect against Alzheimer's disease (AD). However, the underlying mechanisms remain to be elucidated. Recently, microglia dysfunction leading to Aβ clearance impairment is proved an important mechanism for later Aβ deposition and AD pathogenesis. ⋯ Moreover, treadmill exercise partly restored microglial Aβ degradation and clearance in the hippocampus, which was impaired in APP/PS1 mice. However, the impaired microglial Aβ phagocytosis in APP/PS1 mice was not altered after 3 months of treadmill exercise intervention. These findings demonstrate that 3 months of treadmill exercise alleviates hippocampal Aβ deposition and restores spatial learning and memory in APP/PS1 mice, partly by promoting microglial Aβ degradation and clearance.
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Cerebral ischemia/reperfusion is the major pathophysiological process in stroke and could lead to severe and permanent disability. The current study aimed to investigate the effects of dedicator of cytokinesis 2 (DOCK2) on cerebral ischemia/reperfusion-induced cerebral injury. We established a mouse middle cerebral artery occlusion (MCAO) model with suture-occluded method in vivo. ⋯ Subsequently, we found that the loss of DOCK2 upregulated the expression of p-STAT6. DOCK2 knockdown-induced microglial cell polarization towards M2 phenotype was partly abrogated by the STAT6 inhibitor AS1517499. In conclusion, DOCK2 downregulation protected against cerebral ischemia/reperfusion by modulating microglia polarization via the activation of the STAT6 signaling pathway.