Abstract:

Objective To investigate the effects of exogenous brain-derived neurotrophic factor (BDNF) on mechanical pain threshold and astrocytes, and explore the potential mechanism of BDNF-induced pain. Methods Thirty rats with successful intrathecal catheterization were randomly divided into blank control group, placebo group, BDNF group, BDNF+astrocyte inhibitor group (BDNF+fluorocitrate group) and BDNF+tyrosine kinase receptor B(TrkB) inhibitor group (BDNF+K252a group), with 6 rats in each group. Intrathecal administration was performed once daily for 7 d. Fifty percent paw withdrawal threshold (50% PWT) was measured 1 h before each injection. Spinal enlargement parts were obtained 1 h after the last administration, and the expression of glial fibrillary acidic protein (GFAP) and phosphorylated TrkB protein was detected by Western blotting. Results Compared with blank control group, 50% PWT of hind limbs in BDNF group was significantly lower (P<0.05). Seven days after administration, the expression of GFAP and phosphorylated TrkB protein in spinal enlargement parts in BDNF group was significantly higher than that in blank control group (P<0.01). The expression of GFAP protein and 50% PWT in BDNF+ fluorocitrate group and BDNF+K252a group were not significantly different from those in blank control group (P>0.05). There was no significant difference in the expression of phosphorylated TrkB protein between BDNF+K252a group and blank control group (P>0.05). Conclusion BDNF may activate astrocytes via phosphorylated TrkB receptor, which in turn produce neuropathic pain.

Key words: brain-derived neurotrophic factor, glial fibrillary acidic protein, neuropathic pain, phosphorylated tyrosine kinase receptor B, fluorocitrate, K252a