Articles: neuralgia.
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Both early life stress and neuropathic pain induce morphological and functional abnormalities of the nervous system that are associated with emotional regulation. In our previous study, early life stress enhanced nerve injury-induced hyperalgesia in adult male and female mice. In the present study, using phosphorylated extracellular signal-regulated kinase (p-ERK) as a marker of neuronal activation, we examined the effect of early life stress on neuronal function following partial sciatic nerve ligation (PSL). ⋯ The present data suggest that early life stress sex-dependently and site-specifically increases neuronal activity in the brain. In addition, increased neuronal activity in multiplebrain regions of mice subjected to early life stress may enhance hyperalgesia after nerve injury. WHAT DOES THIS STUDY ADD?: Maternal separation and social isolation (MSSI) increased p-ERK in the paraventricular nucleus (PVN) and amygdala of male mice. MSSI increased p-ERK in the medial prefrontal cortex and nucleus accumbens of female mice. Neuropathic pain increased p-ERK in the PVN and amygdala of female MSSI mice.
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Anesthesia and analgesia · Sep 2016
The Antiallodynic Effects of Nefopam Are Mediated by the Adenosine Triphosphate-Sensitive Potassium Channel in a Neuropathic Pain Model.
Nefopam hydrochloride is a centrally acting compound that induces antinociceptive and antihyperalgesic properties in neuropathic pain models. Previous reports have shown that activation of adenosine triphosphate (ATP)-sensitive and calcium-activated potassium (KATP and KCa2+) channels has antiallodynic effects in neuropathic pain. In the present study, we evaluated the relationship between potassium channels and nefopam to determine whether the antiallodynic effects of nefopam are mediated by potassium channels in a neuropathic pain model. ⋯ The antiallodynic effects of nefopam are increased by a KATP channel agonist and reversed by a KATP channel antagonist. These data suggest that the KATP channel is involved in the antiallodynic effects of nefopam in a neuropathic pain model.
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The development of hypersensitivity following spinal cord injury can result in incurable persistent neuropathic pain. Our objective was to examine the effect of red light therapy on the development of hypersensitivity and sensorimotor function, as well as on microglia/macrophage subpopulations following spinal cord injury. ⋯ These findings demonstrate that a simple yet inexpensive treatment regime of red light reduces the development of hypersensitivity along with sensorimotor improvements following spinal cord injury and may therefore offer new hope for a currently treatment-resistant pain condition.
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Chem. Biol. Interact. · Aug 2016
The nitroxyl donor, Angeli's salt, reduces chronic constriction injury-induced neuropathic pain.
Chronic pain is a major health problem worldwide. We have recently demonstrated the analgesic effect of the nitroxyl donor, Angeli's salt (AS) in models of inflammatory pain. In the present study, the acute and chronic analgesic effects of AS was investigated in chronic constriction injury of the sciatic nerve (CCI)-induced neuropathic pain in mice. ⋯ Moreover, chronic AS diminishes CCI-induced mechanical and thermal hyperalgesia by reducing the activation of spinal cord microglia and astrocytes, decreasing TNF-α, IL-1β and IL-33 cytokines expression. This spinal cord immune modulation was more prominent in the chronic treatment with AS. Thus, nitroxyl limits CCI-induced neuropathic pain by reducing spinal cord glial cells activation.
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British dental journal · Aug 2016
Randomized Controlled TrialBotulinum toxin - neuropathic pain: Safety and efficacy of repeated injections of botulinum toxin A in peripheral neuropathic pain (BOTNEP): a randomised, double-blind, placebo-controlled trial.
When treated with botulinum toxin A, those patients with peripheral neuropathic pain and allodynia (triggering of pain from stimuli which do not normally provoke pain) at baseline, would appear to have a better outcome.