European journal of pain : EJP
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Distraction interventions are used clinically to relieve pain. Exposure to distracting stimuli causes withdrawal of attention from the painful stimulus and reduces perceived pain. However, the neurobiological mechanisms mediating distraction-induced analgesia are poorly understood due, in part, to a paucity of animal studies modelling this phenomenon. ⋯ Failure to detect any distractor-induced effects on plasma corticosterone levels or aversive behaviours suggests that the stimuli used were non-stressful. HPLC analysis revealed that there was a significant reduction in serotonin and dopamine metabolites in the medial prefrontal cortex in animals exposed to the novel object. These results indicate that exposure to a novel object or arena reduces nociceptive behaviour in rats, effects accompanied by discrete alterations in serotonin and dopamine metabolites in the medial prefrontal cortex.
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EphrinB-EphB receptor signaling plays diverse roles during development, but recently has been implicated in synaptic plasticity in the matured nervous system and in pain processes. The present study investigated the correlation between expression of ephrinB and EphB receptor proteins and chronic constriction injury (CCI) of the sciatic nerve and dorsal rhizotomy (DR) in dorsal root ganglion (DRG) and spinal cord (SC); and interaction of CCI and DR on expression of these signals. Adult, male Sprague-Dawley rats were employed and thermal sensitivity was determined in the sham operated CCI and DR rats. ⋯ DR suppressed CCI-induced upregulation of ephrinB1 in SC and EphB1 receptor in DRG and SC. These findings indicate that ephrinB-EphB receptor activation and redistribution in DRG and DH neurons after nerve injury could contribute to neuropathic pain. This study may also provide a new mechanism underlying DR-induced analgesia in clinic.
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Antidepressant drugs act mainly by blocking the noradrenaline and/or serotonin uptake sites and require a chronic treatment. Tricyclic antidepressants are among the first line treatments clinically recommended against neuropathic pain. As observed against depression, a chronic treatment is required for a therapeutic effect. ⋯ For comparison, we tested the anticonvulsant gabapentin and showed that it alleviates neuropathic allodynia after 3 days of treatment. Naloxone had no effect on gabapentin therapeutic benefit, showing that antidepressants and anticonvulsants alleviate neuropathic allodynia through independent mechanisms. Our work provides a clinically relevant model to understand the mechanism by which chronic antidepressant treatment can alleviate neuropathic pain.