Neuroscience
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In this review we summarize findings published over the past 10 years focusing on the neural correlates of perceptual decision-making. Importantly, this review highlights only studies that employ a model-based approach, i.e., they use quantitative cognitive models in combination with neuroscientific data. The model-based approach allows capturing latent decision-making processes such as strategic adjustments of response thresholds and relate these to interindividual differences or single-trial blood-oxygenated level dependent (BOLD) functional Magnetic Resonance Imaging (fMRI) responses. ⋯ More concretely, we show that evidence accumulation is associated with a fronto-parietal network which is partly overlapping with choice bias in perceptual decision making. The setting of decision thresholds is associated with fronto-basal ganglia networks which are also found for choice bias. In sum, we argue that the model-based approach holds great promises to understand the neural correlates of latent cognitive processes.
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Chronic exposure to alcohol produces changes in the prefrontal cortex that are thought to contribute to the development and maintenance of alcoholism. A large body of literature suggests that stress hormones play a critical role in this process. Here we review the bi-directional relationship between alcohol and stress hormones, and discuss how alcohol acutely stimulates the release of glucocorticoids and induces enduring modifications to neuroendocrine stress circuits during the transition from non-dependent drinking to alcohol dependence. We propose a pathway by which alcohol and stress hormones elicit neuroadaptive changes in prefrontal circuitry that could contribute functionally to a dampened neuroendocrine state and the increased propensity to relapse-a spiraling trajectory that could eventually lead to dependence.
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Enhanced brain apoptosis (neurons and glia) may be involved in major depression (MD) and schizophrenia (SZ), mainly through the activation of the intrinsic (mitochondrial) apoptotic pathway. In the extrinsic death pathway, pro-apoptotic Fas-associated death domain (FADD) adaptor and its non-apoptotic p-Ser194 FADD form have critical roles interacting with other death regulators such as phosphoprotein enriched in astrocytes of 15 kDa (PEA-15) and extracellular signal-regulated kinase (ERK). The basal status of FADD (protein and messenger RNA (mRNA)) and the effects of psychotropic drugs (detected in blood/urine samples) were first assessed in postmortem prefrontal cortex of MD and SZ subjects (including a non-MD/SZ suicide group). ⋯ Cortical p-PEA-15 was not changed whereas PEA-15 was increased mainly in antidepressant-treated subjects (16-20%). Interestingly, cortical p-ERK1/2/ERK1/2 ratio was reduced (33%) in antidepressant-free when compared to antidepressant-treated MD subjects. The neurochemical adaptations of brain FADD (increased p-FADD and pro-survival p-FADD/FADD ratio), as well as its interaction with PEA-15, could play a major role to counteract the known activation of the mitochondrial apoptotic pathway in MD.
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Interpersonal synchrony is characterized by a temporary alignment of periodic behaviors with another person. This process requires that at least one of the two individuals monitors and adjusts his/her movements to maintain alignment with the other individual (the referent). Interestingly, recent research on interpersonal synchrony has found that people who are motivated to befriend an unfamiliar social referent tend to automatically synchronize with their social referents, raising the possibility that synchrony may be employed as an affiliation tool. ⋯ Overall, our behavioral results showed that the referent of a synchrony task expressed greater perceived synchrony and greater social affiliation toward a synchronous partner (i.e., one displaying low mean asynchrony and/or a narrow asynchrony range) than with an asynchronous partner (i.e., one displaying high mean asynchrony and/or high asynchrony range). Our neuroimaging study extended these results by demonstrating involvement of brain areas implicated in social cognition, embodied cognition, self-other expansion, and action observation as correlates of interpersonal synchrony (vs. asynchrony). These findings have practical implications for social interaction and theoretical implications for understanding interpersonal synchrony and social coordination.
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Evidence is emerging that reactive oxygen species (ROS)-induced oxidative stress has a crucial role in the pathogenesis of neurodegenerative diseases. To find the effective therapies for neurodegenerative diseases, evaluation of the relevant molecular mechanisms is necessary. In the current study, we investigated the effects of hydrogen peroxide (H2O2)-induced oxidative stress on SK-N-MC cell death with focus on HIF-1α, Foxo3a and Notch1 signaling factors. ⋯ In contrast, Notch inhibition resulted in HIF-1α/Foxo3a signaling pathway up-regulation, suggesting the bidirectional crosstalk between HIF-1α and Notch1. These results collectively suggest that ROS are involved in activation of both the defensive and pro-apoptotic pathways encompassing HIF-1α and p53, respectively. Regarding the HIF-1α-mediated neuroprotection role, elucidation of the molecular mechanism would certainly be essential for effective drug design against neurodegenerative diseases.