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However, whetherVGCC<\/jats:styled-content>are involved in pain states driven by abnormalC<\/jats:styled-content>av<\/jats:sub>\u03b12<\/jats:sub>\u03b41<\/jats:sub>expression is not known.<\/jats:p><\/jats:sec>Methods<\/jats:title>Intrathecal injection ofN<\/jats:styled-content>\u2010,P<\/jats:styled-content>\/Q<\/jats:styled-content>\u2010 andL<\/jats:styled-content>\u2010typeVGCC<\/jats:styled-content>blockers were tested in two models: a transgenic neuronalC<\/jats:styled-content>av<\/jats:sub>\u03b12<\/jats:sub>\u03b41<\/jats:sub>overexpression (TG<\/jats:styled-content>) model with behavioural hypersensitivity and a spinal nerve ligation (SNL<\/jats:styled-content>) model withC<\/jats:styled-content>av<\/jats:sub>\u03b12<\/jats:sub>\u03b41<\/jats:sub>overexpression in sensory pathways and neuropathy pain states.<\/jats:p><\/jats:sec>Results<\/jats:title>The nociceptive response to mechanical stimuli was significantly attenuated in both models with \u03c9\u2010conotoxinGVIA<\/jats:styled-content>(anN<\/jats:styled-content>\u2010typeVGCC<\/jats:styled-content>blocker) and nifedipine (anL<\/jats:styled-content>\u2010typeVGCC<\/jats:styled-content>blocker), in which \u03c9\u2010conotoxinGVIA<\/jats:styled-content>appeared more potent than nifedipine. Treatments with \u03c9\u2010agatoxinIVA<\/jats:styled-content>(P<\/jats:styled-content>\u2010VGCC<\/jats:styled-content>blocker), but not \u03c9\u2010conotoxinMVIIC<\/jats:styled-content>(Q<\/jats:styled-content>\u2010VGCC<\/jats:styled-content>blocker) had similar potency in theTG<\/jats:styled-content>model as theN<\/jats:styled-content>\u2010typeVGCC<\/jats:styled-content>blocker, while both \u03c9\u2010agatoxinIVA<\/jats:styled-content>and \u03c9\u2010conotoxinMVIIC<\/jats:styled-content>had minimal effects in theSNL<\/jats:styled-content>model compared with controls.<\/jats:p><\/jats:sec>Conclusion<\/jats:title>These findings suggest that, at the spinal level,N<\/jats:styled-content>\u2010 andL<\/jats:styled-content>\u2010typeVGCC<\/jats:styled-content>are likely involved in behavioural hypersensitivity states driven byC<\/jats:styled-content>av<\/jats:sub>\u03b12<\/jats:sub>\u03b41<\/jats:sub>overexpression.Q<\/jats:styled-content>\u2010typeVGCC<\/jats:styled-content>has minimal effects in both models. The anti\u2010nociceptive effects ofP<\/jats:styled-content>\u2010typeVGCC<\/jats:styled-content>blocker in theC<\/jats:styled-content>av<\/jats:sub>\u03b12<\/jats:sub>\u03b41<\/jats:sub>TG<\/jats:styled-content>mice, but minimally at theSNL<\/jats:styled-content>model with presynapticC<\/jats:styled-content>av<\/jats:sub>\u03b12<\/jats:sub>\u03b41<\/jats:sub>up\u2010regulation, suggest that its potential action site(s) is at the post\u2010synaptic and\/or supraspinal level. These findings support thatN<\/jats:styled-content>\u2010,L<\/jats:styled-content>\u2010 andP<\/jats:styled-content>\/Q<\/jats:styled-content>\u2010typeVGCC<\/jats:styled-content>have differential contributions to behavioural hypersensitivity modulated byC<\/jats:styled-content>av<\/jats:sub>\u03b12<\/jats:sub>\u03b41<\/jats:sub>dysregulation at the spinal cord level.<\/jats:p><\/jats:sec>","DOI":"10.1002\/ejp.585","type":"journal-article","created":{"date-parts":[[2014,8,27]],"date-time":"2014-08-27T09:49:20Z","timestamp":1409132960000},"page":"639-648","source":"Crossref","is-referenced-by-count":22,"title":["Differential effects of voltage\u2010gated calcium channel blockers on calcium channel alpha\u20102\u2010delta\u20101 subunit protein\u2010mediated nociception"],"prefix":"10.1002","volume":"19","author":[{"given":"E.","family":"Chang","sequence":"first","affiliation":[{"name":"Department of Anesthesiology and Perioperative Care University of California Irvine Irvine 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