Neuroscience
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Humans have been consistently shown to be bad at making decisions, especially in disadvantageous situations. In this study, we designed a task that simulates real-life non-strategic gambling to examine the effect of win-lose balance situations (WIN, LOSS, TIE) on decision-making. In behavioral performances, participants showed shorter response time (RT) in LOSS than in WIN and TIE conditions. ⋯ Positive correlation was found between brain activation in IFG and RT in LOSS. Overall, we concluded that, in disadvantageous conditions, participants are frustrated by their negative results and tend to make a random selection without full consideration. In advantageous conditions, participants' motivations to gamble are elicited and they tend to engage in more endeavors in making decisions.
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Type A behavior pattern (TABP) is characterized by competitiveness and hostility, time urgency and impatience. These traits can have a significant impact on physical and mental health. We have not found studies focusing on brain structure or functional connectivity correlates associated with individual differences in TABP. ⋯ In addition, TABP was positively correlated with the strength of rsFC between the left ventral striatum and areas in the left ventromedial prefrontal cortex (vmPFC) and the right rostral anterior cingulate cortex (rACC). These regions are associated with achievement striving related to impatience, aggressiveness, and worry under time pressure. In summary, the combination of morphometric results (increased rGMV of the left sgACC) and functional connectivity findings (increased rsFC between the left ventral caudate and the left vmPFC/right rACC in the fronto-striatal network) may provide a valuable basis for a comprehensive understanding of the neural circuitry underlying individual differences in TABP.
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Myoclonus dystonia syndrome (MDS) is a hyperkinetic movement disorder caused, in a proportion of cases, by mutations of the maternally imprinted epsilon-sarcoglycan gene (SGCE). SGCE mutation rates vary between cohorts, suggesting genetic heterogeneity. E- and ζ-sarcoglycan are both expressed in brain tissue. In this study we tested whether zeta-sarcoglycan gene (SGCZ) mutations also contribute to this disorder. ⋯ SGCZ mutations are unlikely to contribute to the genetic heterogeneity in MDS.
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The anxiolytic diazepam selectively inhibits psychological stress-induced autonomic and behavioral responses without causing noticeable suppression of other central performances. This pharmacological property of diazepam led us to the idea that neurons that exhibit diazepam-sensitive, psychological stress-induced activation are potentially those recruited for stress responses. To obtain neuroanatomical clues for the central stress circuitries, we examined the effects of diazepam on psychological stress-induced neuronal activation in broad brain regions. ⋯ The diazepam treatment significantly reduced the stress-induced Fos expression in many brain regions including the prefrontal, sensory and motor cortices, septum, medial amygdaloid nucleus, medial and lateral preoptic areas, parvicellular paraventricular hypothalamic nucleus, dorsomedial hypothalamus, perifornical nucleus, tuberomammillary nucleus, association, midline and intralaminar thalami, and median and dorsal raphe nuclei. In contrast, diazepam increased Fos-IR cells in the central amygdaloid nucleus, medial habenular nucleus, ventromedial hypothalamic nucleus and magnocellular lateral hypothalamus. These results provide important information for elucidating the neural circuitries that mediate the autonomic and behavioral responses to psychosocial stressors.
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Rivastigmine is a non-competitive inhibitor of both acetylcholinesterase (AChE) and butylcholinesterase (BuChE) used to treat mild to moderate dementia in Alzheimer's disease (AD) patients. Although rivastigmine reportedly ameliorates cognitive dysfunction in these patients, its ability to improve Behavioral and Psychological Symptoms of Dementia (BPSD) remains unclear. To determine whether rivastigmine treatment antagonizes depression-like behaviors, we chronically administered rivastigmine (0.1-1.0mg/kg) to olfactory bulbectomized (OBX) mice once a day for 2weeks, starting 2weeks after bulbectomy. ⋯ These effects were blocked by WAY-100635 but not ketanserin treatment. Finally, we confirmed that 5-HT1A but not 5-HT2A receptor stimulation by specific agonists mimicked rivastigmine-induced anti-depression activity and promoted hippocampal neurogenesis. We conclude that, in addition to enhancing the cholinergic system, rivastigmine treatment restores normal function of the hippocampal serotonergic system, an activity that likely ameliorates depressive behaviors in AD patients.