Neuroscience
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Neural proliferation in the dentate gyrus (DG) is closely linked with learning and memory, but the transcriptional programming that drives adult proliferation remains incompletely understood. Our lab previously elucidated the critical role of the transcription factor ΔFosB in the dorsal hippocampus (dHPC) in learning and memory, and the FosB gene has been suggested to play a role in neuronal proliferation. ⋯ Here, we crossed neurotensin receptor-2 (NtsR2) Cre mice, which express Cre within the subgranular zone (SGZ) of dHPC DG, with floxed FosB mice to show that knockout of ΔFosB in hippocampal SGZ neurons reduces antidepressant-induced neurogenesis and impedes hippocampus-dependent learning in the novel object recognition task. Taken together, these data indicate that FosB gene expression in SGZ is necessary for both hippocampal neurogenesis and memory formation.
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The superior temporal sulcus (STS) encompasses a complex set of regions involved in a wide range of cognitive functions. To understand its functional properties, neuromodulation approaches such brain stimulation or neurofeedback can be used. We investigated whether the posterior STS (pSTS), a core region in the face perception and imagery network, could be specifically identified based on the presence of dynamic facial expressions (and not just on simple motion or static face signals), and probed with neurofeedback. ⋯ Our results provide evidence that a facial expression-selective cluster in pSTS can be identified and may represent a suitable target for neurofeedback approaches, aiming at social and emotional cognition. These findings highlight the presence of a highly selective region in STS encoding dynamic aspects of facial expressions. Future studies should elucidate its role as a mechanistic target for neurofeedback strategies in clinical disorders of social cognition such as autism.
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Early brain injury (EBI) mainly leads to the poor outcome of subarachnoid hemorrhage (SAH), with which inflammation is closely associated. It was reported that triggering receptor expressed on myeloid cells-1 (TREM-1), a critical inflammatory amplifier, increased in cerebrospinal fluid of SAH patients in our recent research. This study was conducted to examine the effects of TREM-1 inhibition on EBI after experimental SAH (eSAH). ⋯ The results showed that TREM-1 was induced in brain after eSAH. Both high dose (3.5 mg/kg) and low dose (1.0 mg/kg) of Lp17 significantly inhibited the induction of TREM-1, but only high dose of LP17 improved neuroscore, brain edema, and BBB disruption which are associated with downregulation of p38MAPK/MMP-9 and subsequent preservation of ZO-1. Overall, the current study provides new evidence that TREM-1 may participate in the pathogenesis of SAH-induced EBI via promoting p38MAPK/MMP-9 activation and ZO-1 degradation, while TREM-1 inhibition attenuated the EBI severity obviously, providing a novel approach for the treatment of EBI.
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High-definition transcranial direct current stimulation (HD-tDCS) is a variant of tDCS, which produces more focal stimulation, delimiting brain current flow to a defined region compared to conventional tDCS. To date, only one study has been conducted to investigate HD-tDCS effects on language recovery in aphasia. Here, we aimed to assess the effects of cathodal HD-tDCS on verb naming by comparing two current intensities: 1 vs 2 mA. ⋯ Our findings showed that HD-tDCS applied to the right intact hemisphere are efficacious for language recovery. These results indicate that HD-tDCS represents a promising new technique for language rehabilitation. However, systematic determination of stimulation intensity appears to be crucial for obtaining relevant effects.
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Binge alcohol drinking is a well characterized consumption pattern related with drinking five or more alcoholic beverages during a short period of time followed by a non-drinking period. Several studies showed that this pattern of alcohol intake is becoming very popular among adolescents. However, little is known about the cellular mechanisms involved in ethanol toxicity under these conditions and if these negative changes could be extending to the adulthood. ⋯ Adolescent binge-like ethanol exposure reduced the expression of the mitochondrial respiration complexes, induced mitochondrial depolarization, increased mitochondrial calcium levels, and reduced ATP production in the adult hippocampus. Altogether, our results indicate that adolescence binge alcohol drinking affects the electron transport chain components expression resulting in mitochondrial failure and loss of calcium buffering in the adult hippocampus. Therefore, we reported for first time that adolescent binge-alcohol consumption has severe repercussions on mitochondrial bioenergetics during the adulthood; and that this is not a transitory change until the state of drunkenness disappears as previously believed.