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      Neuroplastic alteration of TTX-resistant sodium channel with visceral pain and morphine-induced hyperalgesia

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          Abstract

          The discovery of the tetrodotoxin-resistant (TTX-R) Na + channel in nociceptive neurons has provided a special target for analgesic intervention. In a previous study we found that both morphine tolerance and persistent visceral inflammation resulted in visceral hyperalgesia. It has also been suggested that hyperexcitability of sensory neurons due to altered TTX-R Na + channel properties and expression contributes to hyperalgesia; however, we do not know if some TTX-R Na + channel property changes can be triggered by visceral hyperalgesia and morphine tolerance, or whether there are similar molecular or channel mechanisms in both situations. To evaluate the effects of morphine tolerance and visceral inflammation on the channel, we investigated the dorsal root ganglia (DRG) neuronal change following these chronic treatments. Using whole-cell patch clamp recording, we recorded TTX-R Na + currents in isolated adult rat lumbar and sacral (L6−S2) DRG neurons from normal and pathologic rats with colon inflammatory pain or chronic morphine treatment. We found that the amplitudes of TTX-R Na + currents were significantly increased in small-diameter DRG neurons with either morphine tolerance or visceral inflammatory pain. Meanwhile, the result also showed that those treatments altered the kinetics properties of the electrical current (ie, the activating and inactivating speed of the channel was accelerated). Our current results suggested that in both models, visceral chronic inflammatory pain and morphine tolerance causes electrophysiological changes in voltage-gated Na channels due to the chronic administration of these medications. For the first time, the present investigation explored the adaptations of this channel, which may contribute to the hyperexcitability of primary afferent nerves and hyperalgesia during these pathologic conditions. The results also suggest that neurophysiologic mechanisms of morphine tolerance and visceral hyperalgesia are related at the TTX-R Na + channel.

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          Author and article information

          Journal
          J Pain Res
          J Pain Res
          Journal of Pain Research
          Dove Medical Press
          1178-7090
          2012
          08 November 2012
          : 5
          : 491-502
          Affiliations
          [1 ]Department of Internal Medicine, Neuroscience Program, The University of Texas Medical Branch, Galveston, TX, USA
          [2 ]The Divisions of Pharmacy, Pharmacology core lab, MD Anderson Cancer Center, Houston, TX, USA
          [3 ]University of Texas-Pan American, Edinburg, TX, USA
          [4 ]Beijing Institute of Pharmacology and Toxicology, Beijing, China
          Author notes
          Correspondence: Jinghong Chen, Assistant professor in Division of Gastroenterology, Department of Internal Medicine, The University of Texas Medical Branch, 301 University Blvd., Galveston, TX 77555, USA, Tel +1409 747 0678, Fax +1409 772 5841, Email jing.chen@ 123456utmb.edu
          Article
          jpr-5-491
          10.2147/JPR.S27751
          3500918
          23166448
          © 2012 Chen et al, publisher and licensee Dove Medical Press Ltd.

          This is an Open Access article which permits unrestricted noncommercial use, provided the original work is properly cited.

          Categories
          Original Research

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