Articles: hyperalgesia.
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Stress is often a trigger to exacerbate chronic pain including visceral hypersensitivity associated with irritable bowel syndrome, a female predominant functional bowel disorder. Epigenetic mechanisms that mediate stress responses are a potential target to interfere with visceral pain. The purpose of this study was to examine the effect of a histone deacetylase inhibitor, suberoylanilide hydroxamic acid, on visceral hypersensitivity induced by a subchronic stressor in female rats and to investigate the involvement of spinal glutamate receptors. ⋯ In surprising contrast, stress and/or suberoylanilide hydroxamic acid had no effect on spinal NMDA receptor expression or function. These data reveal histone modification modulates mGluR2/3 expression in the spinal cord to attenuate stressinduced visceral hypersensitivity. HDAC inhibitors may provide a potential approach to relieve visceral hypersensitivity associated with irritable bowel syndrome.
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The diagnostic criteria for primary stabbing headache (PSH) in the 3rd beta edition of International Classification of Headache Disorders (ICDH-3 beta) were recently revised. In the ICDH-3 beta, PSH is defined as short-lasting head pain spontaneous occurring as a single stab or series of stabs without autonomic symptoms and involving all head areas (i.e., not limited to the ophthalmic branch region of the trigeminal nerve). The aim of this study was to investigate the validity of the ICHD-3 beta criteria for PSH in a clinic-based setting. ⋯ All patients with headache with stabbing pain without cranial autonomic symptoms fulfilled the diagnostic criteria for PSH according to ICHD-3 beta at the initial visit. Secondary causes for headache with stabbing pain were revealed in a small proportion (3.7 %) of patients after 2 weeks of follow-up.
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Cell transplantation · Jan 2016
Intrathecal Transplantation of Embryonic Stem Cell-Derived Spinal GABAergic Neural Precursor Cells Attenuates Neuropathic Pain in a Spinal Cord Injury Rat Model.
Neuropathic pain following spinal cord injury (SCI) is a devastating disease characterized by spontaneous pain such as hyperalgesia and allodynia. In this study, we investigated the therapeutic potential of ESC-derived spinal GABAergic neurons to treat neuropathic pain in a SCI rat model. Mouse embryonic stem cell-derived neural precursor cells (mESC-NPCs) were cultured in media supplemented with sonic hedgehog (SHH) and retinoic acid (RA) and efficiently differentiated into GABAergic neurons. ⋯ The engrafted spinal GABAergic neurons remarkably increased both the paw withdrawal threshold (PWT) below the level of the lesion and the vocalization threshold (VT) to the level of the lesion (T12, T11, and T10 vertebrae), which indicates attenuation of chronic neuropathic pain by the spinal GABAergic neurons. The transplanted cells were positive for GABA antibody staining in the injured region, and cells migrated to the injured spinal site and survived for more than 7 weeks in L4-L5. The mESC-NPC-derived spinal GABAergic neurons dramatically attenuated the chronic neuropathic pain following SCI, suggesting that the spinal GABAergic mESC-NPCs cultured with low doses of SHH and RA could be alternative cell sources for treatment of SCI neuropathic pain by stem cell-based therapies.
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Cell. Mol. Neurobiol. · Jan 2016
Ligustilide Ameliorates Inflammatory Pain and Inhibits TLR4 Upregulation in Spinal Astrocytes Following Complete Freund's Adjuvant Peripheral Injection.
Ligustilide is a major component of Radix Angelica Sinensis and reported to have anti-inflammatory and anti-nociceptive effects. Toll-like receptor 4 (TLR4) has been shown to be expressed in the spinal cord and be involved in inflammatory pain and neuropathic pain. Whether ligustilide can inhibit spinal TLR4 expression in inflammatory pain is still unknown. ⋯ Immunofluorescence double staining showed that TLR4 was predominantly expressed in spinal astrocytes. In primary cultured astrocytes, ligustilide dose-dependently reduced lipopolysaccharide-induced upregulation of TLR4 mRNA expression. These data indicate that ligustilide treatment reduces TLR4 expression in spinal astrocytes and is an effective therapy for inflammatory pain.
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The contribution of the peripheral nervous system to opiate-induced hyperalgesia (OIH) is not well understood. In this study, we determined the changes in excitability of primary sensory neurons after sustained morphine administration for 7 days. Changes in the expression of glutamate receptors and glutamate transporters after morphine administration were ascertained in dorsal root ganglions. ⋯ Coadministration in vivo of the GluN2B selective antagonist Ro 25-6981 with morphine for 7 days prevented the appearance of OIH and increased morphine-induced analgesia. Administration of morphine for 7 days led to an increased expression of GluN2B and excitatory amino acid transporter 3/excitatory amino acid carrier 1, but not of the α-amino-3-hydroxy-5-methyl-4-isoxazole propionate, kainate, or group I metabotropic glutamate receptors, or of the vesicular glutamate transporter 2. These results suggest that peripheral glutamatergic neurotransmission contributes to OIH and that GluN2B subunit of NMDA receptors in the periphery may be a target for therapy.