Exogenous Acrolein intensifies sensory hypersensitivity after spinal cord injury in rat
Autor: | Breanne Butler, Glen Acosta, Riyi Shi |
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Rok vydání: | 2017 |
Předmět: |
Male
0301 basic medicine Central nervous system Hyperreflexia Pharmacology medicine.disease_cause Rats Sprague-Dawley 03 medical and health sciences chemistry.chemical_compound 0302 clinical medicine Physical Stimulation Administration Inhalation medicine Animals Acrolein Spinal cord injury Spinal Cord Injuries Pain Measurement business.industry Algesia medicine.disease Rats 030104 developmental biology medicine.anatomical_structure Neurology chemistry Hyperalgesia Anesthesia Neuropathic pain Neuralgia Tobacco Smoke Pollution Neurology (clinical) medicine.symptom business 030217 neurology & neurosurgery Oxidative stress |
Zdroj: | Journal of the Neurological Sciences. 379:29-35 |
ISSN: | 0022-510X |
Popis: | Acrolein, an α,β-unsaturated aldehyde associated with oxidative stress, is also a major toxic component of tobacco cigarette smoke, which has been reported in the clinic to coincide with the exacerbation of neuropathic pain after SCI. Previous reports have shown that acrolein involvement in spinal cord injury (SCI) is crucial to the development and persistence of neuropathic pain. Through the activation and upregulation of the transient receptor protein ankyrin-1 (TRPA1) cation channel, acrolein is capable of sensitizing the central nervous system in the acute and chronic stages of SCI. Here, we report that the acute or delayed nasal exposure of acrolein, apart from cigarette smoke but at concentrations similar to that found in cigarette smoke, resulted in increased neuropathic pain behaviors in a rat model of contusion SCI. We also found that this hyperalgesia occurred concurrently with an augmentation in systemic acrolein, detected by an acrolein-glutathione metabolite in the urine. The application of an acrolein scavenger, phenelzine, was shown to reduce the hyperalgesic effect of acrolein inhalation. The previously determined ability of acrolein to bind to and activate the TRPA1 channel and elicit algesic responses may be a mechanism of the phenomenon seen in this study. Upon the exposure to actual cigarette smoke after SCI, intensified neuropathic pain behaviors were also observed and persisted for at least 1 week after the cessation of the exposure period. Taken together, these results indicate that cigarette smoke, through mechanisms involving acrolein, poses a threat to the vulnerable CNS after SCI and can contribute to neuropathic pain. This investigation also provides further evidence for the potential utility of acrolein scavengers as a therapeutic strategy in SCI-resultant neuropathic pain. |
Databáze: | OpenAIRE |
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