Objective     To detect the expression of Rap1a in the spinal cord tissue of rats after spinal nerve ligation (SNL)

determine its effect on neuropathic pain

and investigate the underlying potential mechanism.  Methods      Rat model of SNL were produced by ligating lumbar nerve L5. Then the 60 rats were divided into sham operation group (n=6)

SNL group (n=30)

model+normal saline group (n=6)

model+Cont-shR group (n=6)

model+Rap1a-shR group (n=6)

and model+rapamycin (n=6). Rap1a expression was then detected. Corresponding agents

such as normal saline

adenovirus Rap1a shRNA and others were introduced into the spinal cord tissue of SNL rats by intrathecal injection. The mechanical withdrawal threshold (MWT) of rats was measured by Von-Frey assay. RTPCR and Western blotting were employed to detect the expression of Rap1a

mTOR activity

as well as autophagy in SNL rats and cultured astrocyte.  Results     Compared to the sham operation group

Rap1a expression was significantly up-regulated in the spinal cord tissue of SNL rats

whereas the MWT of the rats was remarkably decreased (P0.05). However

adenovirus Rap1a shRNA infection significantly increased the MWT of SNL rats (P0.05)

and also enhanced the ratio of autophagy maker LC3-Ⅱ/LC3-Ⅰ and reduced the level of p62 in the spinal cord tissue of SNL rats and cultured astrocytes

indicating the increase of autophagy. Besides

the mTOR activity was also decreased by Rap1a shRNA (P0.05). Furthermore

rapamycin dramatically induced the autophagy in the astrocyte and spinal cord tissue as well as the MWT of SNL rats (P0.05).  Conclusion      SNL-induced high expression of Rap1a contributes to the development of neuropathic pain in SNL rats

which might be through activating the mTOR signal pathway and inhibiting the autophagy of astrocyte.