Behavioural brain research
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Comparative Study
Gender associations with chronic methylphenidate treatment and behavioral performance following experimental traumatic brain injury.
Evidence suggests that dopamine (DA) agonists improve cognition after traumatic brain injury (TBI). Methylphenidate (MPH) is a DA agonist that blocks the dopamine transporter (DAT). Moreover, female sex hormones modulate DAT expression. ⋯ Further, injured females treated with MPH had faster swimming speeds than all other groups (P<0.05 all comparisons), and MPH increased activity in TBI females but not males in the FCN task (P<0.05). These results suggest that MPH is beneficial after TBI. However there are gender specific drug differences in behavioral performance and sensitivity to treatment with MPH that may have implications for treatment efficacy and dosing clinically after TBI.
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Stressors increase corticotropin releasing hormone (CRH) functioning in hypothalamic and frontal cortical brain regions, and thus may contribute to the provocation of anxiety and depressive disorder. As the effects of stressors on these behavioral changes are more pronounced in some strains of mice (e.g., BALB/cByJ) than in others (e.g., C57BL/6ByJ), the present investigation assessed whether acute and chronic stressors would differentially influence CRH receptor immunoreactivity (ir-CRHr) and CRH receptor mRNA expression (CRH(1) and CRH(2)) in the orbital frontal cortex (OFC) of these strains. An acute noise stressor, and to a greater extent a chronic, variable stressor regimen reduced ir-CRHr in BALB/cByJ mice. ⋯ The CRH(2) expression appeared in low abundance in both strains and was unaltered by the stressor. In addition to the OFC variations, quantitative immunohistochemistry indicated that the chronic stressor treatment increased CRH immunoreactivity in the median eminence of C57BL/6ByJ mice, but co-expression of CRH and arginine vasopressin (AVP) immunoreactivity was not provoked by the stressors. The data support the view that stressors provoke marked variations of ir-CRHr in the OFC that might contribute to the differential anxiety/depression-like profiles ordinarily apparent in the stressor-vulnerable and -resilient mouse strains.
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Although we demonstrated willed movement (WM) therapy can facilitate the patients actively participating in the physical activities by cognitive and perceptual stimulation in our previous study, the molecular mechanisms of the willed movement on the patients remains unclear. We initially established the model of WM intervention for rats and identified possible effects of willed movement on motor recovery and on expression of Kainate/alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) receptors in ischemia core (IC) and ischemia penumbra (IP) regions of rats after cerebral ischemia reperfusion. ⋯ Early willed movement treatment can increase the expression level of AMPA receptor subunits and thus might increase synaptic transmission and enhance brain plasticity after focal brain ischemia at the subacute stage.