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Previous studies have demonstrated that SCI results in excessive ATP release to the peritraumatic regions and that purinergic signaling, among glial cells, likely plays an essential role in facilitating inflammatory responses and nociceptive sensitization. We sought to assess the role of connexin 43 (Cx43) as a mediator of CNS inflammation and chronic pain. To determine the extent of Cx43 involvement in chronic pain, a weight\u2010drop SCI was performed on transgenic mice with Cx43\/Cx30 deletions. SCI induced robust and persistent neuropathic pain including heat hyperalgesia and mechanical allodynia in wild\u2010type control mice, which developed after 4 weeks and was maintained after 8 weeks. Notably, SCI\u2010induced heat hyperalgesia and mechanical allodynia were prevented in transgenic mice with Cx43\/Cx30 deletions, but fully developed in transgenic mice with only Cx30 deletion. SCI\u2010induced gliosis, detected as upregulation of glial fibrillary acidic protein in the spinal cord astrocytes at different stages of the injury, was also reduced in the knockout mice with Cx43\/Cx30 deletions, when compared with littermate controls. In comparison, a standard regimen of post\u2010SCI treatment of minocycline attenuated neuropathic pain to a significantly lesser degree than Cx43 deletion. These findings suggest Cx43 is critically linked to the development of central neuropathic pain following acute SCI. Since Cx43\/Cx30 is expressed by astrocytes, these findings also support an important role of astrocytes in the development of chronic pain. \u00a9 2012 Wiley Periodicals, Inc.<\/jats:p>","DOI":"10.1002\/glia.22384","type":"journal-article","created":{"date-parts":[[2012,8,3]],"date-time":"2012-08-03T11:54:24Z","timestamp":1343994864000},"page":"1660-1670","source":"Crossref","is-referenced-by-count":176,"title":["Astrocytic CX43 hemichannels and gap junctions play a crucial role in development of chronic neuropathic pain following spinal cord injury"],"prefix":"10.1002","volume":"60","author":[{"given":"Michael 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