The journal of pain : official journal of the American Pain Society
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Endogenous cannabinoids and peripheral cannabinoid CB2 receptors (CB2Rs) are involved in the antinociceptive effect of electroacupuncture (EA) on inflammatory pain. However, it remains unclear about how EA affects the expression and distribution patterns of peripheral CB2Rs in inflamed skin tissues. To study this, inflammatory pain was induced by local injection of complete Freund's adjuvant into the hindpaw of rats. The mRNA and protein levels of CB2Rs were quantified by using RTPCR and Western blotting, respectively. The distribution of CB2Rs on keratinocytes and immune cells recruited to the inflamed skin tissues was determined by using double-immunofluorescence labeling. Induction of tissue inflammation significantly increased the mRNA and protein levels of CB2Rs in the skin tissue. Also, both 2 Hz and 100 Hz EA, applied to GB30 and GB34, significantly increased the mRNA and protein levels of CB2Rs in inflamed tissues compared to the sham EA group. CB2Rimmunoreactivities were mainly distributed in keratinocytes, macrophages, and T-lymphocytes in the epidermis and dermis of the inflamed skin tissue. Inflammation caused a significant increase in the number of CB2R-immunoreactive keratinocytes, macrophages, and T-lymphocytes. Furthermore, compared to the sham EA group, EA at 2 or 100 Hz significantly increased the number of keratinocytes, macrophages, and T-lymphocytes with CB2R-immunoreactivity in the inflamed skin tissue. Therefore, our findings suggest that EA is associated with upregulation of local CB2Rs in the inflamed skin tissue. EA primarily potentiates the expression of CB2Rs on keratinocytes and infiltrating inflammatory cells at the site of inflammation. ⋯ This study shows that electroacupuncture increases the CB2 receptor expression on keratinocytes and infiltrating inflammatory cells in inflammatory skin tissues. This finding provides new evidence showing the potential role of CB2 receptors in the analgesic effect of acupuncture on inflammatory pain.
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Our aim was to describe the referred pain patterns and size of areas of trigger points (TrPs) in the masticatory and neck-shoulder muscles of women with myofascial temporomandibular disorders (TMD). Twenty-five women with myofascial TMD and 25 healthy matched women participated. Bilateral temporalis, deep masseter, superficial masseter, sternocleidomastoid, upper trapezius and suboccipital muscles were examined for TrPs by an assessor blinded to the subjects' condition. TrPs were identified with manual palpation and categorized into active and latent according to proposed criteria. The referred pain areas were drawn on anatomical maps, digitalized, and measured. The occurrence of active (P < .001) and latent TrPs (P = .04) were different between groups. In all muscles, there were significantly more active and latent TrP in patients than controls (P < .001). Significant differences in referred pain areas between groups (P < .001) and muscles (P < .001) were found: the referred pain areas were larger in patients (P < .001), and the referred pain area elicited by suboccipital TrPs was greater than the referred pain from other TrPs (P < .001). Referred pain areas from neck TrPs were greater than the pain areas from masticatory muscle TrPs (P < .01). Referred pain areas of masticatory TrPs were not different (P > .703). The local and referred pain elicited from active TrPs in the masticatory and neck-shoulder muscles shared similar pain pattern as spontaneous TMD, which supports the concept of peripheral and central sensitization mechanisms in myofascial TMD. ⋯ The current study showed the existence of multiple active muscle TrPs in the masticatory and neck-shoulder muscles in women with myofascial TMD pain. The local and referred pain elicited from active TrPs reproduced pain complaints in these patients. Further, referred pain areas were larger in TMD pain patients than in healthy controls. The results are also in accordance with the notion of peripheral and central sensitization mechanisms in patients with myofascial TMD.
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Emotional states have been shown to influence resilient behavior in conditions of loss, bereavement, and stress. Positive affect has been associated with better health outcomes, including chronic pain. Extant research suggests that positive emotions help buffer against stress, suggesting that positive emotions provide an important protective and adaptive significance. This study examined the role of positive versus negative emotions in the association between pain-related coping efficacy and interference with social functioning in a sample of chronic pain patients. Mediational analyses revealed that positive emotions partially mediated the relationship between control and coping efficacy and pain-related interference in social activities. Negative emotions were not found to mediate this relationship. Implications for research on the role of positive emotions in chronic pain are discussed. ⋯ The findings from this study demonstrate the mediating role of positive affect in explaining the relationship between pain-related coping efficacy and interference in social functioning in a sample of chronic pain patients. This could potentially assist clinicians who seek to enhance coping efficacy and social functioning in pain patients.
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The protein kinase mammalian target of rapamycin (mTOR) regulates mRNA translation and is inhibited by rapamycin. Signaling pathways involving mTOR are implicated in physiological and pathophysiological processes. We determined the spinal effects of the rapamycin analogue cell cycle inhibitor (CCI)-779 on neuronal responses and behavioral hypersensitivity in a model of persistent neuropathic pain. We also assessed the anatomical distribution of spinal mTOR signaling pathways. Specifically, we ligated rat spinal nerves L5 and L6 to produce a model of neuropathic pain. After confirming neuropathy with behavioral testing, we obtained in vivo single-unit extracellular stimulus-evoked recordings from deep dorsal horn spinal neurons. We applied CCI-779 spinally in electrophysiological and behavioral studies and assessed its effects accordingly. We also used immunohistochemistry to probe for mTOR signaling pathways in dorsal root ganglia (DRG) and the spinal cord. We found that spinally administered CCI-779 rapidly attenuated calibrated mechanically but not thermally evoked neuronal responses and mechanically evoked behavioral responses. Immunohistochemistry showed presence of mTOR signaling pathways in nociceptive-specific C-fiber DRG and in neurons of inner lamina II of the spinal cord. We conclude that alterations in the activity of spinal mTOR signaling pathways are crucial to the full establishment of spinal neuronal plasticity and behavioral hypersensitivity associated with nerve injury. ⋯ This study is consistent with growing evidence implicating mTOR signaling pathways as important modulators of persistent pain, providing novel insights into the molecular mechanisms of pain maintenance and potential for novel approaches into treating chronic pain.
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The present study examined the hyponociceptive effect of swimming exercise in a chemical behavioral model of nociception and the mechanisms involved in this effect. Male mice were submitted to swimming sessions (30 min/d for 5 days). Twenty-four hours after the last session, we noticed that swimming exercise decreased the number of abdominal constriction responses caused by acetic acid compared with the nonexercised group. The hyponociception caused by exercise in the acetic acid test was significantly attenuated by intraperitoneal (i.p.) pretreatment of mice with naloxone (a nonselective opioid receptor antagonist, 1 mg/kg), ρ-chlorophenylalanine methyl ester (PCPA, an inhibitor of serotonin synthesis, 100 mg/kg once a day for 4 consecutive days), and by bilateral adrenalectomy. Collectively, the present results provide experimental evidences indicating for the first time that high-intensity extended swimming exercise reduces pain-related behavior in mice. The mechanisms involve an interaction with opioid and serotonin systems. Furthermore, endogenous opioids released by adrenal glands probably are involved in this effect. ⋯ Our results indicate that high-intensity extended exercise endogenously controls acute pain by activation of opioidergic and serotonergic pathways. Furthermore, these results support the use of exercise as a nonpharmacological approach for the management of acute pain.