Neuroscience
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Exposure to ethanol in utero is associated with a myriad of sequelae for the offspring. Some of these effects are morphological in nature and noticeable from birth, while others involve more subtle changes to the brain that only become apparent later in life when the individuals are challenged cognitively. One brain structure that shows both functional and structural deficits following prenatal ethanol exposure is the hippocampus. ⋯ Deficits in hippocampal neurogenesis were not apparent in younger animals. Surprisingly, even when ethanol exposure occurred in conjunction with maternal stress, deficits in neurogenesis did not occur at this young age, suggesting that the capacity for neurogenesis is highly conserved early in life. These findings are unique in that they demonstrate for the first time that deficits in neurogenesis associated with prenatal ethanol consumption appear later in life.
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Depression is a worldwide disability disease associated with high morbidity and has increased dramatically in the last few years. The differential diagnosis and the definition of an individualized therapy for depression are hampered by the absence of specific biomarkers. The aim of this study was to evaluate the phospholipidomic profile of the brain and myocardium in a mouse model of depression induced by chronic unpredictable stress (CUS). ⋯ The enzyme activities of catalase (CAT) and superoxide dismutase (SOD) were found to be decreased in the myocardium and increased in the brain, while glutathione reductase (GR) was decreased in the brain. Our results indicate that in a mouse model for studying depression induced by CUS, the modification of the expression of oxidative stress-related enzymes did not prevent lipid oxidation in organs, particularly in the brain. These observations suggest that depression has an impact on the brain lipidome and that further studies are needed to better understand lipids role in depression and to evaluate their potential as future biomarkers.
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Previous studies have indicated a sparse distribution of multisensory neurons in the transition zones between cortical areas associated with specific sensory modalities. However, little is known about the distribution and functional properties of such neurons. The bimodal visual-auditory neurons in the transition area between visual and auditory cortices in rats were examined to determine whether these neurons are modulated by simultaneous input from visual and auditory modalities. ⋯ Exposing adult animals to combined visual and auditory stimuli resulted in an expansion of bimodal neuron distribution in the visual-auditory transition area. These effects were more pronounced in young animals; in this case, the distribution of visual-auditory neurons extended past the limits of the transition area and invaded the flanking modality-specific cortical areas. These results provide a direct demonstration of the role of sensory experience in shaping cortical structure, which can have implications for neuronal integration and cognitive function.
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Sex and reproductive status affect hippocampal neurogenesis and dentate gyrus (DG) size in rodents. Relatively few studies, however, address these two effects simultaneously and even fewer studies address this issue in wild populations. Here, we examined seasonal and sex differences in neurogenesis and DG size in a wild, polygynous and social rodent, Richardson's ground squirrel (Uriocitellus richardsonii). ⋯ Using unbiased stereology and doublecortin (DCX) immunohistochemistry, we found that brain volume, DG size and number of DCX cells varied significantly between breeding and non-breeding seasons, but only brain volume and the number of DCX labeled cells differed between the sexes. Both sex and seasonal differences likely reflect circulating hormone levels, but the extent to which these differences relate to space use in this species is unclear. Based on the degree of seasonal differences in neurogenesis and the DG, we suggest that ground squirrels could be considered model species in which to examine hippocampal plasticity in an ecologically valid context.
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Glutamate-induced excitotoxicity involves a state of acute oxidative stress, which is a crucial event during neuronal degeneration and is part of the physiopathology of neurodegenerative diseases. In this work, we evaluated the ability of sulforaphane (SULF), a natural dietary isothiocyanate, to induce the activation of transcription factor Nrf2 (a master regulator of redox state in the cell) in a model of striatal degeneration in rats infused with quinolinic acid (QUIN). Male Wistar rats received SULF (5mg/kg, i.p.) 24h and 5min before the intrastriatal infusion of QUIN. ⋯ Moreover, SULF treatment increased glutathione peroxidase (GPx) activity, while no changes were observed in γ-glutamyl cysteine ligase (GCL) activity. SULF treatment also prevented QUIN-induced oxidative stress (measured by oxidized proteins levels), the histological damage and the circling behavior. These results suggest that the protective effect of SULF could be related to its ability to preserve GSH levels and increase GPx and GR activities.