Open AccessAttenuated pain responses in mice lacking Ca V 3.2 T‐type channels
Author(s) -
Choi S.,
Na H. S.,
Kim J.,
Lee J.,
Lee S.,
Kim D.,
Park J.,
Chen C.C.,
Campbell K. P.,
Shin H.S.
Publication year - 2007
Publication title -
genes, brain and behavior
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.315
H-Index - 91
eISSN - 1601-183X
pISSN - 1601-1848
DOI - 10.1111/j.1601-183x.2006.00268.x
Subject(s) - nociception , noxious stimulus , chemistry , anesthesia , neuropathic pain , tonic (physiology) , peripheral , medicine , endocrinology , pharmacology , receptor
Although T‐type Ca 2+ channels are implicated in nociception, the function of specific subtypes has not been well defined. Here, we compared pain susceptibility in mice lacking Ca V 3.2 subtype of T‐type Ca 2+ channels (Ca V 3.2 −/− ) with wild‐type littermates in various behavioral models of pain to explore the roles of Ca V 3.2 in the processing of noxious stimuli in vivo . In acute mechanical, thermal and chemical pain tests, Ca V 3.2 −/− mice showed decreased pain responses compared to wild‐type mice. Ca V 3.2 −/− mice also displayed attenuated pain responses to tonic noxious stimuli such as intraperitoneal injections of irritant agents and intradermal injections of formalin. In spinal nerve ligation‐induced neuropathic pain, however, behavioral responses of Ca V 3.2 −/− mice were not different from those of wild‐type mice. The present study reveals that the Ca V 3.2 subtype of T‐type Ca 2+ channels are important in the peripheral processing of noxious signals, regardless of modality, duration or affected tissue type.