Phosphorylation of extracellular signal-regulated kinases in spinal dorsal horn neurons participates in DNFB-induced chronic itch sensation in mice
10.12025/j.issn.1008-6358.2018.20170975
- VernacularTitle:脊髓背角细胞外信号调节激酶磷酸化参与调控2,4-二硝基氟苯诱导的小鼠慢性痒
- Author:
Pin-Wen WU
1
;
Hao ZHANG
;
Hao FANG
Author Information
1. 复旦大学附属中山医院闵行分院麻醉科
- Keywords:
pruritus;
spinal cordorsal horn;
extracellularsignal-regulatekinases;
mice;
inbreICR
- From:
Chinese Journal of Clinical Medicine
2018;25(2):244-248
- CountryChina
- Language:Chinese
-
Abstract:
Objective:To explore whether the activation of extracellular signal-regulated kinases(ERK)signaling in spinal dorsal horn(SDH)neurons participates in DNFB-induced chronic itch sensation.Methods:The ICR male mice,8-12 weeks old,were divided into two groups:DNFB-induced group and acetone control group.The mice in DNFB group were repeatedly smeared with 1.5% DNFB(dissolved by acetone)on the skin of the cheek and the nape to establish the chronic itch model which was analogous to the allergic dermatitis.After DNFB or acetone treatment,the spontaneous scratching behavior was observed and recorded.And the effect of MEK inhibitor U0126 intrathecal injection on the spontaneous scratching behavior was observed.Finally,the perfusion of 4% PFA was performed in mice of DNFB group and control group,the cervical cord segments(C4-C8)were removed,and the expression of pERK was detected by immunofluorescence.Results:In the cheek model,the DNFB-treated mice showed more scratching behavior(86 times in 30 min)than the control mice(17 times in 30 min).In the neck model,compared with the control mice(19 times in 30 min),the DNFB-treated mice showed vigorous scratching behavior(240 times in 30 min).So the chronic neck itch model was successfully established.After the MEK inhibitor U0126 was administered intrathecally at the lumbar level,the scratching behavior of DNFB-treated mice was inhibited obviously.Consistent with the behavior result,the intrathecal injection with U0126 could significantly reduce the number of positive neurons with p-ERK expression at the spinal horn.The activation of pERK was dominantly expressed at lamina Ⅰ andⅡ of spinal horn.In addition,pERK co-expressed with NeuN(a neuron marker),but did not co-expresse with GFAP and Iba1(specific markers for astrocyte and microglia).Conclusions:The phosphorylation of ERK signaling in SDH neurons is required for the regulation of DNFB-induced chronic itch sensation.
