Ablation of IB4 non-peptidergic afferents in the rat facet joint prevents injury-induced pain and thalamic hyperexcitability via supraspinal glutamate transporters.
Ablation of IB4 non-peptidergic afferents in the rat facet joint prevents injury-induced pain and thalamic hyperexcitability via supraspinal glutamate transporters.
复制标题
大鼠刻面关节中IB4非肽性传入的消融可防止损伤引起的疼痛和丘脑性过度刺激性通过上脊髓谷氨酸转运蛋白。
DOI：
10.1016/j.neulet.2017.07.006
复制
发表时间：
2017-08-10
影响因子：
2.5
通讯作者：
Winkelstein BA
中科院分区：
文献类型：
--
作者：
Weisshaar CL;Kras JV;Pall PS;Kartha S;Winkelstein BA
The facet joint is a common source of neck pain, particularly after excessive stretch of its capsular ligament. Peptidergic afferents have been shown to have an important role in the development and maintenance of mechanical hyperalgesia, dysregulated nociceptive signaling, and spinal hyperexcitability that develop after mechanical injury to the facet joint. However, the role of non-peptidergic isolectin-B4 (IB4) cells in mediating joint pain is unknown. Isolectin-B4 saporin (IB4-SAP) was injected into the facet joint to ablate non-peptidergic cells, and the facet joint later underwent a ligament stretch known to induce pain. Behavioral sensitivity, thalamic glutamate transporter expression, and thalamic hyperexcitability were evaluated up to and at day 7. Administering IB4-SAP prior to a painful injury prevented the development of mechanical hyperalgesia that is typically present. Intra-articular IB4-SAP also prevented the upregulation of the glutamate transporters GLT-1 and EAAC1 in the ventral posterolateral nucleus of the thalamus and reduced thalamic neuronal hyperexcitability at day 7. These findings suggest that a painful facet injury induces changes extending to supraspinal structures and that IB4-positive afferents in the facet joint may be critical for the development and maintenance of sensitization in the thalamus after a painful facet joint injury.
登录
查看更多内容
影响因子：
7.4
作者：
Crosby ND;Gilliland TM;Winkelstein BA
通讯作者：
Winkelstein BA
影响因子：
2.5
作者：
Francis, Joseph T.;Xu, Shaohua;Chapin, John K.
通讯作者：
Chapin, John K.
影响因子：
5.3
作者：
Fang, Xin;Djouhri, Laiche;Lawson, Sally N.
通讯作者：
Lawson, Sally N.
影响因子：
64.5
作者：
Basbaum AI;Bautista DM;Scherrer G;Julius D
通讯作者：
Julius D
影响因子：
3.3
作者：
Desantana, J. M.;Da Silva, L. F. S.;De Resende, M. A.;Sluka, K. A.
通讯作者：
Sluka, K. A.