Neuroscience
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Empathy for pain, a widely studied sub-form of empathy, is an ability to recognize and share the pain of others. It involves brain regions associated with the emotional component of pain. Recent studies found that emotional pain could be modulated by stimulating the dorsolateral prefrontal cortex (DLPFC) with transcranial direct current stimulation (tDCS). ⋯ It was found that ratings for others' pain increased in subjects with an anodal tDCS of the DLPFC in comparison to those with sham tDCS, indicating enhanced pain empathy with the anodal tDCS. Furthermore, the changes of ratings for others' pain were positively correlated with the changes of pain-related self-unpleasantness. These findings indicate that tDCS could modulate pain empathy and be used as a potential tool for modulating diseases accompanied with empathy deficits.
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Despite growing interest in meditation as a tool for alternative therapy of stress-related and psychosomatic diseases, brain mechanisms of beneficial influences of meditation practice on health and quality of life are still unclear. We propose that the key point is a persistent change in emotional functioning, specifically the modulation of the early appraisal of motivational significance of events. The main aim was to study the effects of long-term meditation practice on event-related brain potentials (ERPs) during affective picture viewing. ⋯ However, we found no differences in the long latency (400-800ms) responses to emotional images, associated with meditation practice. In addition we found stronger ERP negativity in the time window 200-300ms for meditators compared to the controls, regardless of picture valence. We assume that long-term meditation practice enhances frontal top-down control over fast automatic salience detection, based on amygdala functions.
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Central noradrenergic (NA) signaling contributes critically to multiple behavioral effects of cocaine administration, particularly stress- and anxiety-related effects. The present study examined the ability of acute cocaine to induce the immediate early gene product, cFos, in NA neurons and stress-related neural circuits in rats that were cocaine-naïve, or had a history of cocaine self-administration with or without extinction. Rats implanted with jugular catheters were trained to self-administer cocaine (0.5-mg/kg/infusion), with a subset subsequently trained on extinction. ⋯ Thus, the ability of cocaine to activate central stress circuitry is altered after cocaine self-administration. Our results suggest a unique role for the NTS in cocaine-induced reinstatement, as extinction training enhanced the ability of cocaine to activate NA neurons within this region. These findings suggest central NA systems originating in the caudal brainstem as potential targets for the treatment of cocaine addiction.
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Despite the debilitating consequences and the widespread prevalence of brain trauma insults including spinal cord injury (SCI) and traumatic brain injury (TBI), there are currently few effective therapies for most of brain trauma sequelae. As a consequence, there has been a major quest for identifying better diagnostic tools, predictive models, and directed neurotherapeutic strategies in assessing brain trauma. Among the hallmark features of brain injury pathology is the central nervous systems' (CNS) abnormal activation of the immune response post-injury. ⋯ It is being suggested that there may be an analogy of CNS autoantibodies secretion with the pathophysiology of autoimmune diseases, in which case, understanding and defining the role of autoantibodies in brain injury paradigm (SCI and TBI) may provide a realistic prospect for the development of effective neurotherapy. In this work, we will discuss the accumulating evidence about the appearance of autoantibodies following brain injury insults. Furthermore, we will provide perspectives on their potential roles as pathological components and as candidate markers for detecting and assessing CNS injury.
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Work from the past 40years has unraveled a wealth of information on the cellular and molecular mechanisms underlying synaptic plasticity and their relevance in physiological brain function. At the same time, it has been recognized that a broad range of neurological diseases may be accompanied by severe alterations in synaptic plasticity, i.e., 'maladaptive synaptic plasticity', which could initiate and sustain the remodeling of neuronal networks under pathological conditions. ⋯ This review focuses on recent experimental evidence, which highlights the fundamental role of endoplasmic reticulum-mediated Ca(2+) signals in modulating the duration, direction, extent and type of synaptic plasticity. We discuss the possibility that intracellular Ca(2+) stores may regulate synaptic plasticity and hence behavioral and cognitive functions at the interface between physiology and pathology.