Neuroscience
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Recent studies have explored the circuitry involving the ventral hippocampus (vHPC), the amygdala, and the prefrontal cortex, a pathway mainly activated to store contextual information efficiently. Lesions in the vHPC impair remote memory, but not in the short term. However, how the vHPC is affected by distinct memory strength or its role in systems consolidation has not yet been elucidated. ⋯ The vHPC is required for the expression of remote fear memory and may control contextual fear generalization, a view corroborated by the fact that inactivation of the vHPC suppresses generalized fear expression, making memory more precise again. Systems consolidation occurs concomitantly with greater activation of the vHPC, which is accelerated in stronger fear memories. These findings lead us to propose that greater activation of the vHPC could be used as a marker for memory generalization.
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Ischemic heart disease is a fatal cardiovascular disease that irreversibly impairs the function of the heart, followed by reperfusion leading to a further increase in infarct size. Clinically, we call it myocardial ischemia-reperfusion injury (MIRI). A growing number of clinical observations and experimental studies have found electroacupuncture (EA) to be effective in alleviating MIRI. ⋯ The results were similar to the inhibition of glutamatergic neurons in FN. However, the activation of glutamatergic neurons in FN diminished the aforementioned effects of EA pretreatment. This study revealed that glutamatergic neurons in FN of the cerebellum is involved in EA pretreatment mediated sympathetic nervous and may be a potential mediator for improving MIRI.
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Radiation-induced brain injury (RBI) poses a significant challenge in the context of radiotherapy for intracranial tumors, necessitating a comprehensive understanding of the cellular and molecular mechanisms involved. While prior investigations have underscored the role of astrocyte activation and excessive vascular endothelial growth factor production in microvascular damage associated with RBI, there remains a scarcity of studies examining the impact of radiation on astrocytes, particularly regarding organelles such as mitochondria. Thus, our study aimed to elucidate alterations in astrocyte and mitochondrial functionality following radiation exposure, with a specific focus on evaluating the potential ameliorative effects of translocator protein 18 kDa(TSPO) ligands. ⋯ Moreover, this intervention mitigated astrocyte hyperactivity, decreased the number of A1-type astrocytes, and restored cell proliferative capacity. In conclusion, our study has unveiled additional manifestations of radiation-induced astrocyte dysfunction and validated that TSPO ligands may serve as a promising therapeutic strategy to mitigate this dysfunction. It has potential clinical implications for the treatment of RBI.
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Daily physical activity (dPA) is closely related to circadian rhythm and chronotype. The functional connectivity (FC) within or between the default mode (DMN) and ventral attention network (vAN) were associated with dPA and chronotype. DMN-vAN FC was investigated for its role in chronotype and dPA. 153 participants completed the reduced version of the Morningness-Eveningness Questionnaire (rMEQ), dPA was measured via actigraphy (5-day), and then resting-state fMRI scans were performed. rMEQ scores and steps recorded by the actigraphic devices (with each hour as the time window to calculate steps for five consecutive days per hour, subsequently yielding the maximum number of steps and its corresponding time, ie, SM and SMT) represent chronotype and dPA respectively. ⋯ Further analysis revealed that DMN-vAN mediates the relationship between chronotype and SMT. The FC of DMN-vAN may be the underlying neural mechanism through which chronotype influences dPA. These findings could support the development of reasonable activity schedules or specific intervention programs to improve physical health.
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Intracerebral hemorrhage (ICH), a subtype of devastating stroke, carries high morbidity and mortality worldwide. CircRNA AFF2 (circAFF2) was significantly increased in ICH patients, but the underlying mechanism of circAFF2 is unknown. ⋯ CircAFF2 promotes the injury of neuronal cells and exacerbates ICH via increasing CLSTN3 by sponging miR-488, suggesting that circAFF2 may be a potential therapeutic target for ICH treatment.