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[Phosphorylation of protein kinase C in cerebrospinal fluid-contacting nucleus modulates the inflammatory pain in rats.] [Article in Chinese]

ZHOU Fang, WANG Jia-You, TIAN En-Qi, ZHANG Li-Cai

School of Nursing； Jiangsu Province Key Laboratory of Anesthesiology, Xuzhou Medical College, Xuzhou 221004, China； Anesthesiology Department of the Second Affiliated Hospital of Anhui Medical University, Hefei 230000, China； Department of Anesthesiology, the People’s Hospital of Changzhi, Changzhi 046000, China

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.

Key words: CSF-CN; protein kinase C; inflammatory pain

Received: 2015-07-30　　Accepted: 2015-10-27

Corresponding author: 张励才　　E-mail: licaizhang001@163.com

Citing This Article：

ZHOU Fang, WANG Jia-You, TIAN En-Qi, ZHANG Li-Cai. [Phosphorylation of protein kinase C in cerebrospinal fluid-contacting nucleus modulates the inflammatory pain in rats.] [Article in Chinese]. Acta Physiol Sin 2015; 67 (6): 591-595 (in Chinese with English abstract).