A functional relationship between trigeminal astroglial activation and NR1 expression in a rat model of temporomandibular joint inflammation.
A functional relationship between trigeminal astroglial activation and NR1 expression in a rat model of temporomandibular joint inflammation.
复制标题
颞紧关节炎症大鼠模型中三叉神经胶质细胞激活与NR1表达之间的功能关系。
DOI：
10.1111/j.1526-4637.2012.01511.x
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发表时间：
2012-12
期刊：
影响因子：
--
通讯作者：
Mao J
中科院分区：
文献类型：
--
作者：
Wang S;Song L;Tan Y;Ma Y;Tian Y;Jin X;Lim G;Zhang S;Chen L;Mao J
To examine the hypothesis that glial activation would regulate the expression of the NR1 subunit of the N-methyl-D-aspartate receptor in the trigeminal subnucleus caudalis (Sp5C) after temporomandibular joint (TMJ) inflammation. Inflammation of temporomandibular joint (TMJ) was produced in rats by injecting 50μl complete Freund's adjuvant (CFA) into unilateral TMJ space. Sham control rats received incomplete Freund's adjuvant (IFA) injection. Mechanical nociception in the affected and non-affected TMJ site was tested by using a digital algometer. Fractalkine, fluorocitrate, and/or MK801 were intracisternally administrated to examine the relationship between astroglial activation and NR1 upregulation. CFA TMJ injection resulted in persistent ipsilateral mechanical hyperalgesia 1, 3 and 5 days after CFA injection. The inflammation also induced significant upregulation of CX3CR1 and GFAP beginning on day 1, and of NR1 beginning on day 3, within the ipsilateral Sp5C. Intracisternal administration of fluorocitrate for 5 days blocked the development of mechanical hyperalgesia as well as the upregulation of GFAP and NR1 in the Sp5C. Conversely, intracisternal injection of fractalkine for 5 days exacerbated the expression of NR1 in Sp5C and mechanical hyperalgesia induced by TMJ inflammation. Moreover, once daily intracisternal fractalkine administration for five days in naïve rats induced the upregulation of NR1 and mechanical hyperalgesia. These results suggest that astroglial activation contributes to the mechanism of TMJ pain through the regulation of NR1 expression in Sp5C.
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影响因子：
3.5
作者：
Bradesi S
通讯作者：
Bradesi S
影响因子：
3.3
作者：
Bursztajn, S;Rutkowski, MD;Deleo, JA
通讯作者：
Deleo, JA
影响因子：
2.9
作者：
OKA, T;AOU, S;HORI, T
通讯作者：
HORI, T
影响因子：
3.4
作者：
Pitcher, GM;Henry, JL
通讯作者：
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影响因子：
7.4
作者：
Bereiter, DA;Okamoto, K;Bereiter, DF
通讯作者：
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