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Intrathecal injection of carbenoxolone, a gap junction decoupler, attenuates the induction of below-level neuropathic pain after spinal cord injury in rats.
Exp Neurol. 2010 Jul; 224(1):123-32.EN

Abstract

The most common type of chronic pain following spinal cord injury (SCI) is central neuropathic pain and SCI patients typically experience mechanical allodynia and thermal hyperalgesia. The present study was designed to examine the potential role of astrocyte gap junction connectivity in the induction and maintenance of "below-level" neuropathic pain in SCI rats. We examined the effect of intrathecal treatment with carbenoxolone (CARB), a gap junction decoupler, on SCI-induced bilateral thermal hyperalgesia and mechanical allodynia during the induction phase (postoperative days 0 to 5) and the maintenance phase (days 15 to 20) following T13 spinal cord hemisection. Immunohistochemistry was performed to determine potential SCI-induced changes in spinal astrocyte activation and phosphorylation of the NMDA receptor NR1 subunit (pNR1). CARB administered during the induction period dose-dependently attenuated the development of bilateral thermal hyperalgesia and mechanical allodynia. Intrathecal CARB also significantly reduced the bilateral SCI-induced increase in GFAP-immunoreactive (ir) staining and the number of pNR1-ir cell profiles in the spinal cord dorsal horn compared to vehicle-treated rats. In contrast, CARB treatment during the maintenance phase had no effect on the established thermal hyperalgesia and mechanical allodynia nor on spinal GFAP expression or the number of pNR1-ir cell profiles. These results indicate that gap junctions play a critical role in the activation of astrocytes distant from the site of SCI and in the subsequent phosphorylation of NMDA receptors in the lumbar spinal cord. Both of these processes appear to contribute to the induction of bilateral below-level pain in SCI rats.

Authors+Show Affiliations

Biotherapy Human Resources Center, College of Veterinary Medicine, Chonnam National University, Gwangju, South Korea.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

20226782

Citation

Roh, Dae-Hyun, et al. "Intrathecal Injection of Carbenoxolone, a Gap Junction Decoupler, Attenuates the Induction of Below-level Neuropathic Pain After Spinal Cord Injury in Rats." Experimental Neurology, vol. 224, no. 1, 2010, pp. 123-32.
Roh DH, Yoon SY, Seo HS, et al. Intrathecal injection of carbenoxolone, a gap junction decoupler, attenuates the induction of below-level neuropathic pain after spinal cord injury in rats. Exp Neurol. 2010;224(1):123-32.
Roh, D. H., Yoon, S. Y., Seo, H. S., Kang, S. Y., Han, H. J., Beitz, A. J., & Lee, J. H. (2010). Intrathecal injection of carbenoxolone, a gap junction decoupler, attenuates the induction of below-level neuropathic pain after spinal cord injury in rats. Experimental Neurology, 224(1), 123-32. https://doi.org/10.1016/j.expneurol.2010.03.002
Roh DH, et al. Intrathecal Injection of Carbenoxolone, a Gap Junction Decoupler, Attenuates the Induction of Below-level Neuropathic Pain After Spinal Cord Injury in Rats. Exp Neurol. 2010;224(1):123-32. PubMed PMID: 20226782.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Intrathecal injection of carbenoxolone, a gap junction decoupler, attenuates the induction of below-level neuropathic pain after spinal cord injury in rats. AU - Roh,Dae-Hyun, AU - Yoon,Seo-Yeon, AU - Seo,Hyoung-Sig, AU - Kang,Suk-Yun, AU - Han,Ho-Jae, AU - Beitz,Alvin J, AU - Lee,Jang-Hern, Y1 - 2010/03/11/ PY - 2009/11/11/received PY - 2010/03/01/revised PY - 2010/03/02/accepted PY - 2010/3/16/entrez PY - 2010/3/17/pubmed PY - 2010/6/29/medline SP - 123 EP - 32 JF - Experimental neurology JO - Exp Neurol VL - 224 IS - 1 N2 - The most common type of chronic pain following spinal cord injury (SCI) is central neuropathic pain and SCI patients typically experience mechanical allodynia and thermal hyperalgesia. The present study was designed to examine the potential role of astrocyte gap junction connectivity in the induction and maintenance of "below-level" neuropathic pain in SCI rats. We examined the effect of intrathecal treatment with carbenoxolone (CARB), a gap junction decoupler, on SCI-induced bilateral thermal hyperalgesia and mechanical allodynia during the induction phase (postoperative days 0 to 5) and the maintenance phase (days 15 to 20) following T13 spinal cord hemisection. Immunohistochemistry was performed to determine potential SCI-induced changes in spinal astrocyte activation and phosphorylation of the NMDA receptor NR1 subunit (pNR1). CARB administered during the induction period dose-dependently attenuated the development of bilateral thermal hyperalgesia and mechanical allodynia. Intrathecal CARB also significantly reduced the bilateral SCI-induced increase in GFAP-immunoreactive (ir) staining and the number of pNR1-ir cell profiles in the spinal cord dorsal horn compared to vehicle-treated rats. In contrast, CARB treatment during the maintenance phase had no effect on the established thermal hyperalgesia and mechanical allodynia nor on spinal GFAP expression or the number of pNR1-ir cell profiles. These results indicate that gap junctions play a critical role in the activation of astrocytes distant from the site of SCI and in the subsequent phosphorylation of NMDA receptors in the lumbar spinal cord. Both of these processes appear to contribute to the induction of bilateral below-level pain in SCI rats. SN - 1090-2430 UR - https://www.unboundmedicine.com/medline/citation/20226782/Intrathecal_injection_of_carbenoxolone_a_gap_junction_decoupler_attenuates_the_induction_of_below_level_neuropathic_pain_after_spinal_cord_injury_in_rats_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S0014-4886(10)00071-3 DB - PRIME DP - Unbound Medicine ER -