Chronic inflammation and estradiol interact through MAPK activation to affect TMJ nociceptive processing by trigeminal caudalis neurons.
Chronic inflammation and estradiol interact through MAPK activation to affect TMJ nociceptive processing by trigeminal caudalis neurons.
复制标题
DOI：
10.1016/j.neuroscience.2009.09.058
复制
发表时间：
2009-12-29
期刊：
影响因子：
3.3
通讯作者：
Bereiter, D. A.
中科院分区：
文献类型：
--
作者：
Tashiro, A.;Okamoto, K.;Bereiter, D. A.
The mitogen-activated protein kinase/extracellular regulated kinase (MAPK/ERK) pathway plays a key role in mediating estrogen actions in the brain and neuronal sensitization during inflammation. Estrogen status is a risk factor in chronic temporomandibular muscle/joint disorders (TMJD); however, the basis for this relationship is not known. The present study tested the hypothesis that estrogen status acts through the MAPK/ERK signaling pathway to alter TMJ nociceptive processing. Single TMJ-responsive neurons were recorded in laminae I–II at the spinomedullary (Vc/C1–2) junction in naïve ovariectomized (OvX) female rats treated for 2 days with high (20 μg/day; HE2) or low dose estradiol (2 μg/day; LE2) and after chronic inflammation of the TMJ region by Complete Freund’s Adjuvant (CFA) for 12–14 days. Intra-TMJ injection of ATP (1 mM) was used to activate Vc/C1–2 neurons. The MAPK/ERK inhibitor (PD98059, 0.01–1 mM) was applied topically to the dorsal Vc/C1–2 surface at the site of recording 10 min prior to each ATP stimulus. In naive HE2 rats, low dose PD98059 caused a maximal inhibition of ATP-evoked activity, whereas even high doses had only minor effects on units in LE2 rats. By contrast, after chronic TMJ inflammation, PD98059 produced a marked and similar dose-related inhibition of ATP-evoked activity in HE2 and LE2 rats. These results suggested that E2 status and chronic inflammation acted, at least in part, through a common MAPK/ERK-dependent signaling pathway to enhance TMJ nociceptive processing by laminae I–II neurons at the spinomedullary junction region.
登录
查看更多内容
影响因子：
25
作者：
Ji, RR;Baba, H;Woolf, CJ
通讯作者：
Woolf, CJ
影响因子：
7.4
作者：
Adwanikar, H;Karim, F;Gereau, RW
通讯作者：
Gereau, RW
影响因子：
3.6
作者：
Ioi, Hideki;Kido, Mizuho A.;Tanaka, Teruo
通讯作者：
Tanaka, Teruo
影响因子：
3.3
作者：
GREEN, PG;LUO, J;LEVINE, JD
通讯作者：
LEVINE, JD
影响因子：
2.5
作者：
Iwata, K;Tashiro, A;Ren, K
通讯作者：
Ren, K