Neuroscience
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Subarachnoid hemorrhage due to rupture of intracranial aneurysms has a poor outcome, making this disease being the social problem. Inflammation evoked by the increase in intracranial pressure and the clot in the subarachnoid space after the onset of SAH exacerbates neuronal death and vasospasm, resulting in the poor outcome and severe aftereffects. Here, FROUNT mediates CCR2 and CCR5 signaling as an intracellular molecule binding to these chemoattractant receptors which facilitate the migration of inflammatory cells, such as macrophages, in situ to trigger inflammation there. ⋯ In this condition, disulfiram ameliorated the death of animals after the onset of subarachnoid hemorrhage in rats. In addition, disulfiram suppressed both the two major events after subarachnoid hemorrhage, the neuronal death in hippocampus and vasospasm. The pharmacological inhibition of CCR2 and CCR5 signaling by disulfiram could thus be the therapeutic strategy to improve the outcome of subarachnoid hemorrhage.
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Chronic stress leads to social avoidance and anhedonia in susceptible individuals, a phenomenon that has been observed in both human and animal models. Nevertheless, the underlying molecular mechanisms underpinning stress susceptibility and resilience remain largely unclear. There is growing evidence that epigenetic histone deacetylase (HDAC) mediated histone acetylation is involved in the modulation of depressive-related behaviors. ⋯ Furthermore, HDAC5 overexpression was sufficient to induce depression susceptibility following microdefeat stress, accompanied by a significant reduction in H4K12 level within the hippocampus of mice. Additionally, the Morris water maze (MWM) results indicated that neither CSDS nor HDAC5 exerted significant effects on spatial memory function in mice. Taken together, these investigations indicated that HDAC5-modulated histone acetylation is implicated in regulating the depression susceptibility, and may be serve as potential preventive targets for susceptible individuals.
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Short-term synaptic plasticity refers to the regulation of synapses by their past activity on time scales of milliseconds to minutes. Hippocampal mossy fiber synapses onto CA3 pyramidal cells (Mf-CA3 synapses) are endowed with remarkable forms of short-term synaptic plasticity expressed as facilitation of synaptic release by a factor of up to ten-fold. Three main forms of short-term plasticity are distinguished: 1) Frequency facilitation, which includes low frequency facilitation and train facilitation, operating in the range of tens of milliseconds to several seconds; 2) Post-tetanic potentiation triggered by trains of high frequency stimulation, which lasts several minutes; 3) Finally, depolarization-induced potentiation of excitation, based on retrograde signaling, with an onset and offset of several minutes. ⋯ We then review evidence for a physiological function of short-term plasticity of Mf-CA3 synapses in information transfer between the dentate gyrus and CA3 in conditions of natural spiking, and discuss how short-term plasticity counteracts robust feedforward inhibition in a frequency-dependent manner. Although DG-CA3 connections have long been proposed to play a role in memory, direct evidence for an implication of short-term plasticity at Mf-CA3 synapses is mostly lacking. The mechanistic knowledge gained on short-term plasticity at Mf-CA3 synapses should help in designing future experiments to directly test how this evolutionary conserved feature controls hippocampal circuit function in behavioural conditions.
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Widespread structural changes have been observed in patients with stroke in previous diffusion tensor imaging studies. However, the topological organization of white matter structural networks after acute ischemic stroke (AIS) in the right basal ganglia (BG) remains unknown. The aim of our study is to investigate whether the topological structure of the white matter structural network is altered in patients with AIS in the right BG, and its relationship with cognition. ⋯ Reduced structural connectivity detected by NBS in AIS patients were primarily located in the lesional hemisphere. Furthermore, altered nodal properties were correlated with cognitive scores. Documenting the alterations in the topological patterns of white matter structural networks will help to promote the understanding of the neural mechanisms of cognitive impairment after AIS in the right BG.
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Cancer and depression are closely interrelated, particularly in patients with advanced cancer, who often present with comorbid anxiety and depression for various reasons. Recently, there has been a growing interest in the study of depression in cancer patients, with the aim of assessing the possible triggers, predictors, adverse events, and possible treatment options for depression in several common cancers. The objective of this narrative review is to synthesize the extant literature on the relationship between the occurrence and progression of depression in several common patient categories. ⋯ The current research findings indicate a strong association between cancer and depression. However, the direction of causality remains unclear. Focusing on depression in cancer patients may, therefore, be beneficial for these patients.