Neuroscience
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Traumatic brain injury (TBI) is one of the leading causes of death and disability in children and adolescents. The neuropathological sequelae that result from TBI are a complex cascade of events including edema formation, which occurs more frequently in the pediatric than the adult population. This developmental difference in the response to injury may be related to higher water content in the young brain and also to molecular mechanisms regulating water homeostasis. ⋯ In contrast, AQP1 levels distant from the injury site were increased at 7, 30, and 60 days within septal neurons but did not correlate with changes in edema formation. Group differences were not observed for AQP9. Overall, our observations confirm that astrocyticAQP4 plays a more central role than AQP1 or AQP9 during the edema process in the young brain.
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Exposure to ethanol during the prenatal period contributes to increased alcohol consumption and preference in rodents and increased risk for alcoholism in humans. With studies in adult animals showing the orexigenic peptides, enkephalin (ENK), galanin (GAL) and orexin (OX), to stimulate ethanol consumption, the question addressed here is whether prenatal ethanol alters the development in utero of specific neurons that express these peptides. With reports describing suppressive effects of high doses of ethanol, we examined the offspring of dams gavaged from embryonic day 9 to parturition with a control solution or lower ethanol doses, 1 and 3g/kg/day, known to promote ethanol consumption in the offspring. ⋯ These BrdU-positive neurons were found to express ENK, GAL and OX, indicating that prenatal ethanol promotes neurogenesis in these specific peptide systems. There were no changes in gliogenesis or apoptosis. This increase in neurogenesis and density of peptide-expressing neurons suggests the involvement of these hypothalamic and accumbal peptide systems in mediating the increased alcohol consumption observed in prenatal ethanol-exposed offspring.
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Brain-implantable electrodes such as those used in deep brain stimulation (DBS) have a promising future in end-stage Parkinson's disease therapy. However, there is considerable injury when electrodes penetrate brain tissue. For instance, broken blood vessels and glial scar formation may impede continual DBS or electrical recording from specific neurons. ⋯ We also found that resveratrol not only provided almost complete protection from mechanical injury to the brain, but that it also prevented undesirable motor deficits often seen in animals with lesions to the STN. Lastly, continuous infusion of resveratrol over a 4-week period led to the inhibition of pro-apoptotic, neurodegenerative and cell division cycle genes that may be associated with a reduction in astrocytic gliosis and glial scar formation within the STN. Taken together, these data suggest that application of resveratrol to the brain is an effective adjunct surgical procedure for minimizing acute neuronal injury when electrodes are implanted directly into the STN.
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Motor imagery (MI) refers to the mental simulation of a movement. It is used as a tool to improve motor function in several populations. In young adults, it has been repeatedly shown that MI of upper-limb movements is facilitated when one's posture is congruent with the movement to simulate. ⋯ The present findings extend to walking movements the notion that adopting a posture congruent with the movement to imagine facilitates the simulation process. They also suggest that, at least for simple walking tasks, this effect is maintained across the lifespan. The implication of our findings for optimizing MI training of locomotor-related activities is underlined.
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Diabetes mellitus (DM) is a major stroke risk factor and is associated with poor recovery compared with nondiabetic stroke patients. In the present study, we investigated the effects of tissue plasminogen activator (tPA) treatment of stroke in diabetic and non-diabetic rats. ⋯ Treatment of stroke with tPA increased brain hemorrhage, BBB leakage and failed to improve functional outcome in T1DM rats. The increased inflammatory response may contribute to the failed neuroprotective effects of tPA treatment in T1DM rats.