Spinal D-amino acid oxidase contributes to mechanical pain hypersensitivity induced by sleep deprivation in the rat
| Autor: | Ai-Niu Ma, Antti Pertovaara, Jin-Lu Huang, Xin-Yan Li, Hong Wei, Yong-Xiang Wang, Hui Fan, Nian Gong |
|---|---|
| Rok vydání: | 2013 |
| Předmět: |
D-Amino-Acid Oxidase
Male Pain Threshold Clinical Biochemistry Rapid eye movement sleep Pain Sleep REM Pharmacology Toxicology Biochemistry Nitric oxide 03 medical and health sciences Behavioral Neuroscience chemistry.chemical_compound 0302 clinical medicine medicine Animals Rats Wistar Biological Psychiatry 030304 developmental biology chemistry.chemical_classification 0303 health sciences Reactive oxygen species Oxidase test Behavior Animal Dose-Response Relationship Drug Rats Sleep deprivation medicine.anatomical_structure Spinal Cord chemistry Anesthesia Hyperalgesia Pyrazoles Sleep Deprivation medicine.symptom 030217 neurology & neurosurgery Endogenous agonist Astrocyte |
| Zdroj: | Pharmacology Biochemistry and Behavior. 111:30-36 |
| ISSN: | 0091-3057 |
| Popis: | We studied the hypothesis that spinal d-amino acid oxidase (DAAO) that is expressed in astrocytes and that has been reported to promote tonic pain in various pathophysiological conditions plays a role in 'physiological' pain hypersensitivity induced by rapid eye movement sleep deprivation (REMSD). The experiments were performed in healthy rats with a chronic intrathecal (i.t.) catheter. Pain behavior was assessed by determining limb withdrawal response to repetitive stimulation of the hind paw with a calibrated series of monofilaments. REMSD of 48 h duration produced a significant mechanical hypersensitivity. At 48 h of REMSD, the animals were treated i.t. with a DAAO inhibitor or vehicle. Three structurally different DAAO inhibitors were tested in this study: 6-chlorobenzo[d]isoxazol-3-ol (CBIO), sodium benzoate, and 5-methylpyrazole-3-carboxylic acid (AS-057278). CBIO (1-3 μg), sodium benzoate (30-100 μg) and AS-057278 (3-10 μg) produced dose-related antihypersensitivity effects in sleep-deprived animals. In control animals (with no sleep deprivation), the currently used doses of DAAO inhibitors failed to produce significant changes in mechanically evoked pain behavior. The results indicate that among spinal pain facilitatory mechanisms that contribute to the sleep deprivation-induced mechanical pain hypersensitivity is DAAO, presumably due to production of reactive oxygen species, such as hydrogen peroxide, an endogenous agonist of the pronociceptive TRPA1 ion channel. |
| Databáze: | OpenAIRE |
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