The journal of pain : official journal of the American Pain Society
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This study aims to 1) examine the temporal influence of peer victimization on mood, sleep quality, pain, and activity limitations in clinical and community samples of youth, and 2) test mood and sleep as mediators of peer victimization-pain pathways. One hundred fifty-six adolescents (n = 74 chronic pain group) completed a week of online diary monitoring assessing their daily peer victimization experiences, negative mood, sleep quality, pain intensity, and pain-related activity limitations. In multilevel models controlling for group status, person-mean peer victimization (averaged across days) significantly predicted worse mood, pain, and activity limitations (all Ps < .01) while daily victimization predicted worse mood (P < .05). ⋯ Peer victimization is associated with negative health indicators in clinical and community samples of youth and may exert its influence on pain and pain-related activity limitations through negative mood. PERSPECTIVE: This article examines the temporal influence of peer victimization on pain in adolescents with and without chronic pain, and examines mood and sleep quality as mechanisms linking victimization to pain. This information may be useful for pain prevention researchers as well as providers who assess and treat pain in childhood.
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Numerous studies have demonstrated a physiological interaction between the mu opioid receptor (MOR) and delta opioid receptor (DOR) systems. A few studies have shown that dual MOR-DOR agonists could be beneficial, with reduced tolerance and addiction liability, but are nearly untested in chronic pain models, particularly neuropathic pain. In this study, we tested the MOR-DOR agonist SRI-22141 in mice in the clinically relevant models of HIV Neuropathy and Chemotherapy-Induced Peripheral Neuropathy (CIPN). ⋯ Overall, these results provide compelling evidence that MOR-DOR agonists could have strong efficacy with reduced side effects and an anti-inflammatory mechanism in the treatment of neuropathic pain. PERSPECTIVE: This study demonstrates that a MOR-DOR dual agonist given chronically in chronic neuropathic pain models has enhanced efficacy with strongly reduced tolerance and dependence, with a further anti-inflammatory effect in the spinal cord. This suggests that MOR-DOR dual agonists could be effective treatments for neuropathic pain with reduced side effects.
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The anterior cingulate cortex (ACC) modulates emotional responses to pain. Whereas, the caudal ACC (cACC) promotes expression of pain affect, the rostral ACC (rACC) contributes to its suppression. Both subdivisions receive glutamatergic innervation, and the present study evaluated the contribution of N-methyl-d-aspartic acid (NMDA) receptors within these subdivisions to rats' expression of pain affect. ⋯ These findings demonstrate that NMDA receptor agonism within the cACC and rACC either increases or decreases emotional responses to noxious stimulation, respectively. PERSPECTIVE: NMDA receptor activation of the rostral and caudal ACC respectively inhibited or enhanced rats' emotional response to pain. These findings mirror those obtained from human neuroimaging studies; thereby, supporting the use of this model system in evaluating the contribution of ACC to pain affect.
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Vincristine, oxaliplatin, and cisplatin are commonly prescribed chemotherapeutic agents for the treatment of many tumors. However, a main side effect is chemotherapy-induced peripheral neuropathy (CIPN), which may lead to changes in chemotherapeutic treatment. Although symptoms associated with CIPN are recapitulated by mouse models, there is limited knowledge of how these drugs affect the expression of genes in sensory neurons. ⋯ Treatment with cisplatin resulted in a mixed gene expression signature. PERSPECTIVE: These results provide insight into the recruitment of immune responses to dorsal root ganglia and indicate enhanced neuroinflammatory processes following administration of vincristine, oxaliplatin, and cisplatin. These gene expression signatures may provide insight into novel drug targets for treatment of CIPN.