Neuroscience
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Much attention has been focused on physical exercise benefits to mental health such as mood and cognitive function. Our recent studies have consistently shown that a single bout of exercise elicits increased task-related brain activation mainly in the dorsolateral part of the prefrontal cortex (DLPFC), which results in improved executive performance. As the DLPFC is associated with the modulation of mood as well as executive function, it is tempting to hypothesize that exercising while in a positive mood would facilitate the beneficial effects of exercise on executive function via DLPFC activation. ⋯ Contrary to our hypothesis, there were no significant differences between conditions in improvement in Stroop task performance and task-related cortical activation in the left-DLPFC. The correlation analyses, however, revealed significant correlations among increased vitality, shortened Stroop interference time and increased activation in the left-DLPFC. These results support the hypothesis that positive mood while exercising influences the benefit of exercise on prefrontal activation and executive performance.
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Rodents' behavioural analysis can be influenced by several factors, including housing. The PhenoWorld (PhW) is an enriched housing and testing paradigm, which proved to be relevant for screening depressive-like behaviours in rats, being remarkably sensitive for hedonic behaviour. ⋯ The NAc volumes and NAc medium spiny neurons branching tend also to be higher in animals experiencing the physical enrichment provided in the PhW, but significant differences were not found between animals living in PhW compared to animals living in standard cages (STD6). These results demonstrate that living in a more naturalistic complex environment, closer to real life experience, impacts on the structure of brain regions implicated in complex multidimensional disorders.
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Steroid hormones secreted by the gonads (sex steroids) and adrenal glands (glucocorticoids, GC) are known to influence brain structure and function. While levels of sex steroids wane in late adulthood, corticosteroid levels tend to rise in many individuals due to age-related impairments in their feedback on central mechanisms regulating adrenal function. These fluctuations in sex and adrenal steroid secretion may be relevant to age-related neurodegenerative disorders such as Alzheimer's disease (AD) in which hyperphosphorylation of Tau protein is a key pathological event. ⋯ Interestingly, we observed that the changes in Tau induced by manipulation of the GC milieu of male rats were exacerbated by testosterone depletion (by orchiectomy). While this finding supports previous suggestions of a neuroprotective role of male sex hormones, this is the first study to address interactions between adrenal and sex steroids on Tau hyperphosphorylation and accumulation that are known to endanger neuronal function and plasticity. These results are particularly important for understanding the mechanisms that can precipitate AD because, besides being modulated by age, GC are elevated by stress, a phenomenon now established as a trigger of deficits in neural plasticity and survival, cognitive behaviour and AD-like Tau pathology.
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Astrocytes are now known to play crucial roles in the central nervous system, supporting and closely interacting with neurons and therefore able to modulate brain function. Both human postmortem studies in brain samples from patients diagnosed with Major Depressive Disorder and from animal models of depression reported numerical and morphological astrocytic changes specifically in the hippocampus. In particular, these studies revealed significant reductions in glial cell density denoted by a decreased number of S100B-positive cells and a decrease in GFAP expression in several brain regions including the hippocampus. ⋯ Both antidepressants decreased astrocytic complexity immediately after stress exposure. Moreover, we show that astrocytic alterations, particularly an increased number of S100B-positive cells, are observed after recurrent stress exposure. Interestingly, these alterations were prevented at the long-term by either fluoxetine or imipramine treatment.
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The consequences of excessive fructose intake extend beyond those of metabolic disorder to changes in emotional regulation and cognitive function. Long-term consumption of fructose, particularly common when begun in adolescence, is more likely to lead to deleterious consequences than acute consumption. These long-term consequences manifest differently in males and females, suggesting a sex-divergent mechanism by which fructose can impair physiology and neural function. ⋯ When exposed to an acute energetic challenge, the pattern was reversed. Taken together, these data indicate that diet-induced alterations to neural function and physiology are sex-specific and highlight the need to consider sex as a biological variable when treating metabolic disease. Furthermore, these data suggest that synaptic mitochondrial function may contribute directly to the behavioral consequences of elevated fructose consumption.