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Opioid\u2010based medications are initially effective for acute pain, but tolerance to their analgesic effects quickly develops, and long\u2010term use often leads to physical dependence and addiction. Furthermore, neuropathic pain is generally resistant to non\u2010steroidal anti\u2010inflammatory drugs. Other classes of medications including antidepressants, antiepileptics and voltage\u2010gated calcium channel inhibitors are only partially effective in most patients, may be associated with significant side effects and have few disease\u2010modifying effects on the underlying pathology. Medications that act through new mechanisms of action, and particularly ones that have disease\u2010modifying properties, would be highly desirable. In the last decade, a potential new target for the treatment of neuropathic pain has emerged: the \u03b19\u2010containing nicotinic acetylcholine receptor (nAChR). Recent studies indicate that antagonists of \u03b19\u2010containing nAChRs are analgesic in animal models of neuropathic pain. These nerve injury models include chronic constriction injury, partial sciatic nerve ligation, streptozotocin\u2010induced diabetic neuropathy and chemotherapeutic\u2010induced neuropathy. This review details the history and state of the field regarding the role that \u03b19\u2010containing nAChRs may play in neuropathic pain. An alternative hypothesis that \u03b1\u2010conotoxins exert their therapeutic effect through blocking N\u2010type calcium channels via activation of GABA<jats:sub>B<\/jats:sub> receptors is also reviewed. Understanding how antagonists of \u03b19\u2010containing nAChRs exert their therapeutic effects may ultimately result in the development of medications that not only treat but also prevent the development of neuropathic pain states.<\/jats:p><\/jats:sec><jats:sec><jats:title>Linked Articles<\/jats:title><jats:p>This article is part of a themed section on Nicotinic Acetylcholine Receptors. To view the other articles in this section visit <jats:ext-link xmlns:xlink=\"http:\/\/www.w3.org\/1999\/xlink\" xlink:href=\"http:\/\/onlinelibrary.wiley.com\/doi\/10.1111\/bph.v175.11\/issuetoc\">http:\/\/onlinelibrary.wiley.com\/doi\/10.1111\/bph.v175.11\/issuetoc<\/jats:ext-link><\/jats:p><\/jats:sec>","DOI":"10.1111\/bph.13931","type":"journal-article","created":{"date-parts":[[2017,6,29]],"date-time":"2017-06-29T19:28:00Z","timestamp":1498764480000},"page":"1915-1927","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":75,"title":["\u03b19\u2010containing nicotinic acetylcholine receptors and the modulation of pain"],"prefix":"10.1111","volume":"175","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-9912-0955","authenticated-orcid":false,"given":"Arik J","family":"Hone","sequence":"first","affiliation":[{"name":"Department of Biology University of Utah  Salt Lake City UT USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Denis","family":"Servent","sequence":"additional","affiliation":[{"name":"Service d'Ing\u00e9nierie Mol\u00e9culaire des Prot\u00e9ines (SIMOPRO), IBITECS, CEA Universit\u00e9 Paris\u2010Saclay  Gif\u2010sur\u2010Yvette France"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"J Michael","family":"McIntosh","sequence":"additional","affiliation":[{"name":"Department of Biology University of Utah  Salt Lake City UT USA"},{"name":"George E. 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