Pain
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Pain captures attention, displaces current concerns, and prioritises escape and repair. This attentional capture can be measured by its effects on general cognition. Studies on induced pain, naturally occurring acute pain, and chronic pain all demonstrate a detrimental effect on specific tasks of attention, especially those that involve working memory. ⋯ Furthermore, we also found an effect of pain intensity; performance was poorer in participants with higher intensity compared with that in those with lower intensity pain. We suggest that the effects of pain on attention found in the laboratory occur in more naturalistic settings. Pain is common in the general population, and such interruption may have important, as yet uninvestigated, consequences for tasks of everyday cognition that involve working memory, such as concentration, reasoning, motor planning, and prospective memory.
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The anterolateral tract (ALT), which originates from neurons in lamina I and the deep dorsal horn, represents a major ascending output through which nociceptive information is transmitted to brain areas involved in pain perception. Although there is detailed quantitative information concerning the ALT in the rat, much less is known about this system in the mouse, which is increasingly being used for studies of spinal pain mechanisms because of the availability of genetically modified lines. The aim of this study was therefore to determine the extent to which information about the ALT in the rat can be extrapolated to the mouse. ⋯ However, we also observed certain species differences, in particular we found that many spinoparabrachial cells in laminae III and IV lack the NK1r, meaning that they cannot be identified based solely on the expression of this receptor. We also provide evidence that the majority of spinoparabrachial cells are glutamatergic and that some express substance P. These findings will be important for studies designed to unravel the complex neuronal circuitry that underlies spinal pain processing.
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Nuclear factor-kappa B (NF-κB) signaling is implicated in both cancer development and inflammation processes. However, the roles and mechanisms of NF-κB signaling in the development of cancer-induced pain (CIP) remain unknown. This study was designed to investigate the roles of the p65 subunit of NF-κB in regulation of the purinergic receptor (P2X3R) plasticity in dorsal root ganglion (DRG) of CIP rats. ⋯ Interestingly, tumor cell injection led to a significant demethylation of CpG island in p2x3r gene promoter and enhanced ability of p65 to bind the promoter of p2x3r gene. Our findings suggest that upregulation of P2X3R expression was mediated by the enhanced binding capability of p65 with demethylated promoter of p2x3r gene, thus contributing to CIP. NF-κBp65 might be a potential target for treating CIP, a neuropathic pain generated by tumor cell-induced injury to nerves that innervate the skin.