Phosphorylation of protein kinase C in cerebrospinal fluid-contacting nucleus modulates the inflammatory pain in rats.
- Author:
Fang ZHOU
1
;
Jia-You WANG
2
;
En-Qi TIAN
2
;
Li-Cai ZHANG
3
Author Information
1. School of Nursing, Xuzhou Medical College, Xuzhou 221004, China.
2. Jiangsu Province Key Laboratory of Anesthesiology, Xuzhou Medical College, Xuzhou 221004, China.
3. Jiangsu Province Key Laboratory of Anesthesiology, Xuzhou Medical College, Xuzhou 221004, China. licaizhang001@163.com.
- Publication Type:Journal Article
- MeSH:
Animals;
Freund's Adjuvant;
Inflammation;
enzymology;
Neurons;
enzymology;
Pain;
enzymology;
Phosphorylation;
Protein Kinase C;
cerebrospinal fluid;
chemistry;
Rats;
Rats, Sprague-Dawley
- From:
Acta Physiologica Sinica
2015;67(6):591-595
- CountryChina
- Language:Chinese
-
Abstract:
The present study was aimed to investigate the role of cerebrospinal fluid-contacting nucleus (CSF-CN) neurons in modulation of inflammatory pain and underlying mechanism. The inflammatory pain model was made by subcutaneous injection of the complete Freund's adjuvant (CFA) into the left hind paw of rats. The phosphorylation level of PKC (p-PKC) was examined by Western blot. Thermal withdrawal latency (TWL) of the rats was measured to assess inflammatory pain. The results showed that, compared with the sham controls, the inflammatory pain model rats showed shortened TWL on day 1, 3, and 7 after CFA injection, as well as increased level of p-PKC in CSF-CN neurons at 24 h after CFA injection. The administration of GF109203X, a PKC inhibitor, into lateral ventricle decreased the level of p-PKC protein expression and increased TWL in the model rats. These results suggest that blocking the PKC pathway in CSF-CN neurons may be an effective way to reduce or eliminate the inflammatory pain.
