Behavioural brain research
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It is thought that a close dialogue between the primary motor (M1) and somatosensory (S1) cortices is necessary for skilled motor learning. The extent of the relative S1 contribution in producing skilled reaching movements, however, is still unclear. Here we used anodal transcranial direct current stimulation (tDCS), which is able to alter polarity-specific excitability in the S1, to facilitate skilled movement in intact behaving rats. ⋯ Bilateral BiAno1 stimulation was associated with greater qualitative functional improvement than unilateral UnAno stimulation. tDCS-induced improvements were not observed in the after-effects phase. Quantitative cytoarchitectonic analysis revealed that somatosensory tDCS bilaterally increases cortical neural density. The findings emphasize the central role of bilateral somatosensory feedback in skill acquisition through modulation of cortico-motor excitability.
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Both epidemiologic and laboratory studies suggest that parents can shape their offspring's development. Recently, it has been shown that maternal exercise during pregnancy benefits the progeny's brain function. However, little is known regarding the influence of paternal exercise on their offspring's phenotype. ⋯ Immunohistochemistry staining, real time-PCR and western blot were performed to determine hippocampal BDNF and reelin expression of the male pups after behavior tasks. Our results showed that paternal treadmill exercise improved the spatial learning and memory capability of male pups, which was accompanied by significantly increased expression of BDNF and reelin, as compared to those of C group. Our results provide novel evidence that paternal treadmill exercise can enhance the brain functions of their F1 male offspring.
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Many patients with chronic inflammatory disorders have an abnormal high prevalence of major depression accompanied by elevated levels of tumor necrosis factor-α (TNF-α). We hypothesize that systemic TNF-α increases brain monoamine metabolism, which might induce anhedonia (i.e. a core symptom of major depression). The effect of an intraperitoneal TNF-α injection on extracellular monoamine and metabolite concentrations was investigated by in vivo microdialysis in the nucleus accumbens (NAc) of C57BL/6 mice. ⋯ Remarkably, TNF-α also increased the dopamine metabolite HVA, without affecting dopamine levels itself. These data concur with earlier findings that pro-inflammatory cytokines enhance serotonin transporter activity, and possibly also dopamine transporter activity in the brain. However, more research is needed to understand the precise molecular mechanisms by which TNF-α increases transporter activity and anhedonia.
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The study of individual differences provides an important methodological approach to analyze the neurobehavioral spectrum of a given cohort in order to understand brain function and disease. Based on immobility time in the forced swimming test (FST) juvenile and adult rats were classified as subgroups with low and high immobility. Afterwards, we compared behavior, neurochemical parameters, and gene expression profiles in some brain areas of rats with low and high immobility only. ⋯ Moreover, the expression of accumbal corticotrophin-releasing factor receptor 1 (CRFR1) was significantly different in animals with low and high immobility at both ages, with animals less immobile showing higher levels of CRFR1 mRNA levels. Taken together, our findings suggest that differences in monoaminergic neurotransmission and CRFR1 expression are associated with the coping strategy adopted by the animal and with the tendency to develop depression-related behaviors. Concerning monoaminergic neurotransmission such association is modulated by age, and such modulation could be related to the differential behavioral results observed between juvenile and adult rats.
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Anandamide and 2-arachidonoylglycerol (2-AG) are the two main endocannabinoids, exerting their effects by activating type 1 (CB1r) and type 2 (CB2r) cannabinoid receptors. Anandamide inhibits anxiety-like responses through the activation of CB1r in certain brain regions, including the dorsolateral periaqueductal gray (dlPAG). 2-AG also attenuates anxiety-like responses, although the neuroanatomical sites for these effects remained unclear. Here, we tested the hypothesis that enhancing 2-AG signaling in the dlPAG would induce anxiolytic-like effects. ⋯ These behavioral responses were prevented by CB1r (AM251) or CB2r (AM630) antagonists. Our results showed that the augmentation of 2-AG levels in the dlPAG induces anxiolytic-like effects. The mechanism seems to involve both CB1r and CB2r receptors.