Brain research
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Higher-order processing of nociceptive input is distributed in corticolimbic regions of the brain, including the anterior cingulate, parieto-insular and prefrontal cortices, as well as subcortical structures such as the bed nucleus of stria terminalis and amygdala. In addition to their role in pain processing, these regions encode or modulate emotional, motivational and sensory responses to stress. Thus, pain and stress pathways in the brain intersect at cortical and subcortical forebrain structures. ⋯ Defeated rats exhibited a significant increase in cold preference after social defeat compared to the baseline. In the escape task, the rats exhibited increased escape from warm and nociceptive cold and heat temperatures. Thus, chronic social stress produces hyperalgesia for both hot and cold stimuli in male rats, suggesting a mutually facilitatory cross-regulation between central pathways regulating stress and pain.
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In this study, we evaluated the expression of MCP-1 in the rat dorsal root ganglion (DRG) and spinal cord following axotomy and chronic constriction injury (CCI) of the sciatic nerve and L5 spinal nerve ligation (L5 SNL) using an immunohistochemical approach. MCP-1 expression in the DRG peaked and declined before the full onset of pain hypersensitivity following nerve injury. Spinal expression of MCP-1 peaked when mechanical allodynia was maximal, but then declined rapidly despite the remarkable persistence of mechanical allodynia. ⋯ Despite increased MCP-1 in small and large DRG neurons, a remarkable increase in MCP-1-IR terminals was observed in the spinal superficial laminae following CCI and L5SNL, but not following axotomy; however, in the deeper laminae, a considerable increase in MCP-1-IR terminals, which may originate from the large and injured L5 DRG neurons, was found after L5 SNL. Our results demonstrate that MCP-1 synthesized in DRG neurons may or may not be transported to the spinal cord depending on the type of peripheral nerve injury. Additionally, increased MCP-1 in both intact L4 and injured L5 DRG neurons may contribute to neuropathic pain hypersensitivity following L5 SNL.
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Our recent magnetoencephalography study demonstrated that the mu rhythm can reliably indicate sensorimotor resonance during the perception of pain in others (Cheng, Y., Yang, C. Y., Lin, C. P., Lee, P. ⋯ Further, the mu suppression for pain empathy was positively correlated with the scoring on the personal distress subscale of the interpersonal reactivity index only in the female participants. The present findings suggest the existence of a gender difference in pain empathy in relation with the sensorimotor cortex resonance. The mu rhythm can be a potential biomarker of empathic mimicry.
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Secondary brain damage plays a critical role in the outcome of patients with traumatic brain injury (TBI). The multiple mechanisms underlying secondary brain damage, including posttraumatic cerebral ischemia, glutamate excitotoxicity, oxidative stress, calcium overload and inflammation, are associated with increased mortality and morbidity after head injury. TBI is documented to have detrimental effects on mitochondria, such as alterations in glucose utilization and the depression of mitochondrial oxidative phosphorylation. ⋯ The differences may indicate the degree of metabolic and physiologic dysfunction. Our results will better define the roles of gene expression and metabolic function in long-term prognosis and outcome after TBI. With a considerable understanding of post-injury mitochondrial dysfunction, therapeutic interventions targeted to the mitochondria may prevent secondary brain damage that leads to long-term cell death and neurobehavioral disability.
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This neuroimaging study investigated the neural mechanisms of the effect of conversation on visual event detection during a driving-like scenario. The static load paradigm, established as predictive of visual reaction time in on-road driving, measured reaction times to visual events while subjects watched a real-world driving video. Behavioral testing with twenty-eight healthy volunteers determined the reaction time effects from overt and covert conversation tasks in this paradigm. ⋯ We identified a frontal-parietal network that maintained event detection performance during the conversation task while watching the driving video. Increased brain activations for conversation vs. no conversation during such simulated driving was found not only in language regions (Broca's and Wernicke's areas), but also specific regions in bilateral inferior frontal gyrus, bilateral anterior insula and orbitofrontal cortex, bilateral lateral prefrontal cortex (right middle frontal gyrus and left frontal eye field), supplementary motor cortex, anterior and posterior cingulate gyrus, right superior parietal lobe, right intraparietal sulcus, right precuneus, and right cuneus. We propose an Asynchrony Model in which the frontal regions have a top-down influence on the synchrony of neural processes within the superior parietal lobe and extrastriate visual cortex that in turn modulate the reaction time to visual events during conversation while driving.