Open AccessRole of the oestrogen receptors GPR30 and ERα in peripheral sensitization: relevance to trigeminal pain disorders in women
Author(s) -
Liverman CS,
Brown JW,
Sandhir R,
McCarson KE,
Berman NEJ
Publication year - 2009
Publication title -
cephalalgia
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.57
H-Index - 125
eISSN - 1468-2982
pISSN - 0333-1024
DOI - 10.1111/j.1468-2982.2008.01789.x
Subject(s) - medicine , gper , peripheral , sensitization , relevance (law) , receptor , neuroscience , estrogen receptor , immunology , breast cancer , psychology , cancer , political science , law
Oestrogen increases facial allodynia through its actions on activation of the MAPK extracellular‐signal regulated kinase (ERK) in trigeminal ganglion neurons. This goal of study was to determine which oestrogen receptor is required for behavioural sensitization. Immunohistochemical studies demonstrated the presence of oestrogen receptor alpha (ERα) in nuclei of larger neurons and cytoplasm of smaller neurons, and the novel oestrogen receptor G‐protein coupled receptor 30 (GPR30) in small diameter neurons that also contained peripherin, a marker of unmyelinated C‐fibres. Specific agonists for ERα (PPT) and GPR30 (G‐1), but not ERβ (DPN), activated ERK in trigeminal ganglion neurons in vitro . Both G‐1 and PPT treatment increased allodynia after CFA injections into the masseter of ovariectomized Sprague–Dawley rats. Treatment with oestrogen increased expression of ERα but not GPR30, while masseter inflammation increased GRP30 but not ERα. Differential modulation of these ERK‐coupled receptors by oestrogen and inflammation may play a role in painful episodes of temporomandibular disorder and migraine.