Pain
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We aimed to examine the effects of contextual factors (ie, observers' training background and priming texts) on decoding facial pain expressions of younger and older adults. A total of 165 participants (82 nursing students and 83 nonhealth professionals) were randomly assigned to one of 3 priming conditions: (1) information about the possibility of secondary gain (misuse); (2) information about the frequency and undertreatment of pain in the older adult (undertreatment); or (3) neutral information (control). Subsequently, participants viewed 8 videos of older adults and 8 videos of younger adults undergoing a discomforting physical therapy examination. ⋯ By contrast, priming observers with the misuse text attenuated their valence ratings towards younger patients. Finally, the undertreatment prime influenced observers' pain estimates indirectly through observers' valence towards patients. In summary, results add specificity to the theoretical formulations of pain by demonstrating the influence of patient and observer characteristics, as well as informational primes, on decoding pain expressions.
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Ongoing pain has been linked to ongoing activity (OA) in human C-fiber nociceptors, but rodent models of pain-related OA have concentrated on allodynia rather than ongoing pain, and on OA generated in non-nociceptive Aβ fibers rather than C-fiber nociceptors. Little is known about how ongoing pain or nociceptor OA is generated. To define neurophysiological alterations underlying nociceptor OA, we have used isolated dorsal root ganglion neurons that continue to generate OA after removal from animals displaying ongoing pain. ⋯ Can DSFs also be enhanced acutely to promote OA in neurons from uninjured animals? A low dose of serotonin failed to change resting membrane potential but lowered action potential threshold. When combined with artificial depolarization to model inflammation, serotonin also strongly potentiated DSFs and OA. These findings reveal nociceptor specializations for generating OA that may promote ongoing pain in chronic and acute conditions.
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Tobacco smoking is particularly evident in individuals experiencing chronic pain. This complex relationship is poorly understood at both molecular and behavioral levels. Here, we describe experiments aimed at understanding whether a chronic pain state induces neuroadaptations into the brain or peripheral nerves that involve nicotinic acetylcholine receptors (nAChRs) and whether these neuroadaptations directly lead to increased vulnerability to nicotine addiction or to the development of coping strategies to relieve pain symptoms. ⋯ Spinal nerve ligation and sham rats were equally sensitive to nicotine-induced anxiety-like behavior and antinociception; however, nicotine produced a potent and long-lasting antiallodynic effect in spinal nerve ligation rats. These results demonstrate that chronic pain leads to plasticity of nAChRs that do not directly facilitate nicotine addictive behaviors. Instead, nicotine potently decreases allodynia, an effect that could lead to increased nicotine consumption in chronic pain subjects.