Neuroscience
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Characterizing the functional involvement of specific brain regions has long been a central challenge in cognitive neuroscience. Functional magnetic resonance imaging (fMRI) techniques have offered solutions for mapping functional neural networks. The complex nature of structure-function correspondence makes an elaborate task design difficult to fully capture higher-order cognitive function. ⋯ Just like looking up a "coordinate-based cognition dictionary", researchers can receive a plethora of related tb-fMRI activation information characterized by cognitive domains, specific cognitive functions, cognitive task paradigms, and related publications. Surprisingly, we found that only less than 1% of brain-behavior association or between-group comparison studies have utilized this dictionary approach. We encourage the community to further engage with the existing databases for specific and comprehensive interpretation of neuroimaging as well as guidance of future experimental tb-fMRI design.
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Alterations in cognitive functions, social behaviors and stress reactions are commonly diagnosed in chronic mental illnesses (CMI). Animal models expressing mutant genes associated to CMI represent either rare mutations or those contributing only minimally to genetic risk. Non-genetic causes of CMI can be modeled by disturbing downstream signaling pathways, for example by inducing protein misassembly or aggregation. ⋯ Additionally, there was a trend towards increased corticosterone levels after restraint stress in the tgDISC1 rats. Our findings suggest that DISC1 protein misassembly leads to disturbances of cognitive flexibility and social behaviors, and might also be involved in stress sensitization. Since the observed behavioral features resemble symptoms of CMI, the tgDISC1 rat may be a valuable model for the investigation of cognitive, social and - possibly - also stress-related symptoms of major mental illnesses.
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High school students who participate in contact sports are vulnerable to sustaining multiple concussions and exhibit deficits in cognitive function in both the acute and chronic phases and in emotional behavior in the chronic phase. Further, boys are more likely to suffer cognitive problems whereas girls tend to report depression and anxiety. The effects of repetitive mild TBI in adolescent (35-40-day old) male and female Sprague-Dawley rats on object location and spatial working memory (hippocampal-dependent) and object recognition memory (hippocampal-independent) at 1-and-4-weeks post-injury along with trait-dependent anxiety- and depressive-like behaviors at 5 weeks were examined. ⋯ In contrast, depressive-like behaviors were present in the forced swim test in only the female brain-injured animals at 5 weeks post-injury; anxiety-like behaviors were not evident in either male or female brain-injured animals. Histological analysis at 6 weeks after injury revealed that repeated mild TBI in male and female adolescent rats resulted in increased reactivity of astrocytes and microglia within the corpus callosum below the impact site and in the stratum oriens and stratum pyramidale of the CA2 region of the dorsal hippocampus. Together, these data are indicative of the differences in the temporal pattern of post-traumatic behavioral deficits between male and female animals and that female animals may be more likely to develop deficits in the chronic post-traumatic period.
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There is a high level of comorbidity between depression and alcohol use disorder. Subanesthetic doses of ketamine induce short-acting and enduring antidepressant effects after a single or a few administrations. Considering such comorbidity, we assessed, in Swiss male mice, if ketamine-induced antidepressant-like effects would alter ethanol's rewarding effects; and, if ethanol pretreatment would alter the rewarding and antidepressant effects of ketamine. ⋯ Ketamine (50 mg/kg) induced hippocampal downregulation of 145 kDa TrkB may contribute to ketamine-induced antidepressant tolerance. Likewise, a relationship between low hippocampal levels of p75NTR in the Ethanol-Ketamine (50 mg/kg) and ketamine-induced CPP blockade may be considered. The findings underscore potential ethanol-ketamine interactions likely to undermine ketamine putative antidepressant effects.