Brain research
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Early recovery from incomplete spinal cord contusion is improved by prolonged stimulation of the hindbrain's serotonergic nucleus raphe magnus (NRM). Here we examine whether increases in cyclic adenosine monophosphate (cAMP), an intracellular signaling molecule with several known restorative actions on damaged neural tissue, could play a role. Subsequent changes in cAMP-dependent phosphorylation of protein kinase A (PKA) and PKA-dependent phosphorylation of the transcription factor "cAMP response element-binding protein" (CREB) are also analyzed. ⋯ The phosphorylated fraction of PKA (pPKA) and CREB (pCREB) was reduced significantly in all three regions after SCI and restored by NRM stimulation, except for pCREB in lumbar segments. In conclusion, SCI produces spreading deficits in cAMP, pPKA and pCREB that are reversible by Gs protein-coupled 5-HT receptors responding to raphe-spinal activity, although these signaling molecules are not reactive to NRM stimulation in normal tissue. These findings can partly explain the benefits of NRM stimulation after SCI.
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Convincing evidence indicates that inflammation contributes to the adverse prognosis of subarachnoid hemorrhage (SAH). Some pro-inflammatory molecules such as high mobility group protein 1, S100 family of proteins, β-amyloid peptide, and macrophage antigen complex 1 have been involved in the damaging inflammation process following SAH. The receptor for advanced glycation end-products (RAGE) is a transmembrane receptor that senses these molecules and plays central role in inflammatory processes. ⋯ Moreover, there was a significant positive correlation between the expression of RAGE and that of p65 protein. Double immunofluorescence staining showed that RAGE was expressed by neuron and microglia rather than astrocyte after SAH. These results suggest that RAGE may be directly involved in the inflammatory response after SAH, and there might be important implications for further studies using specific RAGE antagonists to decrease inflammation-mediated brain injury following SAH.
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The aim of the present study was to identify, whether and how oral hormonal contraceptives (OCs) alter women's number processing. Behavioral performance and brain activation patterns (BOLD-response) of 14 OC-users were evaluated during two distinct numerical tasks (number comparison, number bisection) and compared to 16 men (high testosterone), and 16 naturally cycling women, once during their follicular (low hormone levels) and once during their luteal cycle phase (high progesterone). For both tasks, reliable sex differences and menstrual cycle dependent modulation have previously been described. ⋯ Our findings suggest that OC-users resemble follicular women in their behavioral performance, but show male-like brain activation patterns during both tasks. Analysis of brain-behavior relationships suggests that OC-users differ from naturally cycling women in the way they recruit their neural resources to deal with challenges of the tasks. We conclude that OCs, which are used by 100 million women worldwide, may have profound effects on cognition that have not been recognized so far.
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This study addressed the engagement of attention and working memory, as inferred from electrophysiological measurements, in the processing of small sets of objects. We recorded N2pc and CDA, two lateralized components of the EEG signal associated respectively with individuation and visual working memory, while participants enumerated a variable number (1-9) of uniquely colored targets among distractors. ⋯ However, individual differences in the enumeration efficiency were correlated only with the individual variation in the N2pc modulations. The results suggest that the constraints of the attentional individuation system play a significant role in the occurrence of the subitizing phenomenon.
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Nogo-A is a major form of growth inhibitory molecule (growth-IM) which inhibits axonal regeneration and neurite regrowth after neural injury. Bone marrow stromal cells (MSCs) have been shown to inhibit Nogo-A expression in vitro and in cerebral ischemic animal models. The present study was designed to investigate the effects of treatment with human MSCs (hMSCs) impregnated into collagen scaffolds on the expression of Nogo-A and axonal plasticity after traumatic brain injury (TBI). ⋯ In addition, scaffold+hMSC transplantation decreased Nogo-A transcription in oligodendrocytes after TBI. Scaffold+hMSC treatment was superior to hMSC-alone treatment in suppressing Nogo-A expression and enhancing axonal regeneration after TBI. Our data suggest that transplanting hMSCs with scaffolds down-regulates Nogo-A transcription and protein expression which may partially contribute to the enhanced axonal regeneration after TBI.