Brain research
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Comparative Study
The effects of hypertonic saline and nicotinamide on sensorimotor and cognitive function following cortical contusion injury in the rat.
Hypertonic saline (HTS) is an accepted treatment for traumatic brain injury (TBI). However, the behavioral and cognitive consequences following HTS administration have not thoroughly been examined. Recent preclinical evidence has suggested that nicotinamide (NAM) is beneficial for recovery of function following TBI. ⋯ HTS-treated animals showed a greater loss of hippocampal tissue compared to the other groups. In general, NAM showed a faster rate of recovery than HTS without this associated tissue loss. The results of this study reiterate the strengths of NAM following injury and show concerns with bolus administrations of HTS due to the differential effects on cognitive performance and apparent tissue loss.
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Structural and functional alterations of the putamen have been reported in patients with attention deficit hyperactivity disorder (ADHD), but the functional relationships between this area and other brain regions are seldom explored. In the present study, seed-based correlation analyses were performed in the resting-state functional magnetic resonance imaging (fMRI) data to examine the differences in functional connectivity of the putamen between medication-naïve children with ADHD and normal children. ⋯ For children with ADHD, areas exhibiting decreased positive functional connectivity with left putamen-ROI were seen in right frontal and limbic regions, and regions showing decreased negative connectivity with the putamen-ROIs were observed in areas belonging to the default mode network (for left putamen-ROI, including right cerebellum and right temporal lobe; for right putamen-ROI, including left cerebellum and right precuneus). The above results suggest that abnormal functional relationships between the putamen and the cortical-striatal-thalamic circuits as well as the default mode network may underlie the pathological basis of ADHD.
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Maternal glucocorticoid treatment reduces blood-brain permeability early, but not late in fetal development, and pretreatment with glucocorticoids does not affect barrier permeability in newborn lambs. In addition, endogenous increases in plasma cortisol levels are associated with decreases in blood-brain barrier permeability during normal fetal development. Therefore, we tested the hypotheses that development as well as endogenous and exogenous glucocorticoids alters the expression of tight junction proteins in the cerebral cortex of sheep. ⋯ Claudin-5 was higher in dexamethasone than placebo-treated lambs, and ZO-2 was higher in fetuses of dexamethasone than placebo-treated ewes at 90% gestation. ZO-2 expression demonstrated a direct correlation with increases in plasma cortisol during fetal development. We conclude that claudin-1, claudin-5, ZO-1, and ZO-2 expression exhibit differential developmental regulation, exogenous glucocorticoids regulate claudin-5 and ZO-2 in vivo at some, but not all ages, and increases in endogenous fetal glucocorticoids are associated with increases in ZO-2 expression, but not with occludin, claudin-1, claudin-5 or ZO-1 expression in ovine cerebral cortices.
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Both pro-nociceptive and antinociceptive mediators are released in the tissues during inflammation. Balance of these two types of mediators determines the induction and maintenance of pain or hypernociception. This study was designed to explore whether 5-HT(2A) receptors in the periphery contributed to the maintenance of carrageenan-evoked hyperalgesia. ⋯ The hypoalgesia was completely abolished by local or systemic injection of naloxone methiodide. The present study suggests that 5-HT(2A) receptors were involved in the maintenance of inflammatory pain, and that 5-HT suppressed inflammation-associated endogenous opioid analgesia contributing to its pro-nociceptive actions in the periphery. It implied a possible therapeutic benefit of blockade of local 5-HT(2A) receptors in the treatment of inflammatory pain.
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The combination of hyperbaric oxygen therapy (HBO) and recombinant tissue-plasminogen activator (tPA) is of interest in the treatment of acute ischemic stroke with a view to combine positive effects of both strategies. We investigated neurological and functional outcome after early treatment with HBO additional to tPA in ischemic stroke. Focal cerebral ischemia was induced using an embolic stroke model in 87 male Wistar rats. ⋯ This first report of early simultaneous treatment with tPA and HBO in experimental embolic stroke with 4-week follow-up confirms previous studies reporting positive effects of HBO shortly after the ischemia. Following the acute phase, combined tPA and HBO resulted in deterioration of neurological deficits without affecting functional recovery. Future studies should focus on interactions of tPA and HBO on molecular level leading to delayed damage to brain tissue at risk.