Neuroscience
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Thioredoxin family proteins are key modulators of cellular redox regulation and have been linked to several physiological functions, including the cellular response to hypoxia-ischemia. During perinatal hypoxia-ischemia (PHI), the central nervous system is subjected to a fast decrease in O2 and nutrients with a subsequent reoxygenation that ultimately leads to the production of reactive species impairing physiological redox signaling. Particularly, the retina is one of the most affected tissues, due to its high oxygen consumption and exposure to light. ⋯ Knock-down of Trx1 in ARPE-19 cells affected cell morphology, proliferation and the levels of specific differentiation markers. Administration of recombinant Trx1 decreased astrogliosis and improved delayed neurodevelopment in animals exposed to PHI. Taken together, our results suggest therapeutical implications for Trx1 in retinal damage induced by hypoxia-ischemia during birth.
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Fluoro-Jade C (FJC) staining is widely used for the specific detection of all degenerating mature neurons, including apoptotic, necrotic, and autophagic cells. However, whether FJC staining can detect degenerating immature neurons and neural stem/precursor cells remains unclear. In addition, some conflicting studies have shown that FJC and its ancestral dyes, Fluoro-Jade (FJ) and FJB, can label resting/activated astrocytes and microglia. ⋯ Surprisingly degenerating mesenchymal cells were also FJC(+). The present study indicates that FJC is a reliable marker for degenerating neuronal cells during all differentiation stages. However, FJC could also label degenerating non-neuronal cells under some conditions.
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The ventral hippocampus is a component of the neural circuitry involved with context-associated memory for reward and generation of appropriate behavioral responses to context. Glycogen synthase kinase 3 beta (GSK3β) has been linked to the maintenance of synaptic plasticity, contextual memory retrieval, and is involved in the reconsolidation of cocaine-associated contextual memory. In this study, the effects of targeted downregulation of GSK3β in the ventral hippocampus were examined on a series of behavioral tests for assessing drug reward-context association and non-reward related memory. ⋯ Impaired object location memory was observed in mice with GSK3β downregulation in the ventral hippocampus, but novel object recognition remained intact. These results indicate that GSK3β signaling in the ventral hippocampus is differentially involved in the formation of place-drug reward association dependent upon drug class. Additionally, ventral hippocampal GSK3β signaling is important in detection of discrete spatial cues, but not recognition memory for objects.
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Motor expertise has recently been associated with differences in domain-general cognition. Studies using averaged neurophysiological signals (e.g., event-related potentials) have shown varying degree of expertise-related differences in neural activity. As a result, the precise mechanisms underlying these differences remain to be described. ⋯ The interceptive sport players showed superior behavioral performance overall on the task relative to the static sport players. Although both groups exhibited greater sample entropy across most time scales in high-conflict relative to low-conflict trials over the parietal site, this effect was only evident at coarser time scales over the midfrontal site for the interceptive sport players. Together, our results suggest that individual differences in motor expertise may be associated with difference in information-processing capacity and information integration during cognitive processing, as demonstrated by differential cognitive modulation of brain signal variability.
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The gene associated with retinoid-interferon-induced mortality-19 (GRIM-19) plays several significant roles in cellular processes, including ATP synthesis, reactive oxygen species formation, and the regulation of glycolytic enzyme activity, which are closely related to the pathophysiological mechanisms of epilepsy. Therefore, we investigated the expression pattern of GRIM-19 in the CA1 area of the hippocampus in 8-week-old male C57BL/6 mice following pilocarpine-induced status epilepticus (SE). Neuronal death in the hippocampal CA1 area was prominently observed at 4 and 7 days after SE, and astrocytes and microglia became progressively activated beginning at 1 day after SE. ⋯ Moreover, we observed that both GRIM-19 and pyruvate kinase isozyme M2, a glycolytic enzyme, were highly expressed in reactive astrocytes after SE. These results indicate that expression of GRIM-19 in the hippocampus is mainly observed in neurons under normal conditions but is altered in the SE mouse model as evidenced by its increased expression in reactive astrocytes. The possible role of GRIM-19 in the glycolytic activity of reactive astrocytes is also discussed.