Pain threshold of rats with spared nerve injury and changes of TRPA1 mRNA expression in spinal dorsal root ganglion

Objective To observe the pain threshold of spared nerve injury (SNI) rats and the transient receptor potential cation channel subfamily A member 1 (TRPA1) mRNA expression of dorsal root ganglion (DRG) in the 4th cervical vertebra and the 5th cervical vertebra in rats at different time points after modeling; and to discuss the significance of peripheral TRPA1 mRNA in different stages of neuropathic pain model. Methods Thirty healthy adult male Sprague-Dawley rats, weighing 200-230 g, were selected and randomly divided into three groups: control group (6 cases), sham operation group (6 cases) and spared nerve injury model group (SNI group, 18 cases). In SNI group, the left common peroneal nerve and the sacral nerve were ligated, but the sural nerve was preserved. In the sham operation group, the skin muscles were dissected and the nerves were not ligated, and the incision was directly sutured. Rats in control group were not given any treatments. All rats were tested for bilateral hind limb mechanical withdrawal threshold (MWT) 3 days and 1 day before surgery, and 1, 3, 5, 7, 9, 12, 14 days after surgery. Three rats were sacrificed in sham operation group and control group, respectively. At 1, 3, 5, 7 and 14 days after treatment, 3 rats of SNI group were sacrificed everyday. The DRGs in the 4th cervical vertebra and the 5th cervical vertebra of the rats were taken and the expression of TRPA1 mRNA was detected by quatitative-polymerase chain reaction (q-PCR). Results The MWT values of the left hind limbs in SNI group were decreased progressively after SNI, which were significantly different from sham operation group (P 0.05). Compared with the sham operation group, the level of TRPA1 mRNA was significantly increased 1 day and 3 days after SNI, and the TRPA1 mRNA was significantly decreased 7 days after surgery (P<0.01). Conclusions SNI model rats have neuropathic pain. Peripheral TRPA1 mRNA participates in the generation and maintenance of pain in SNI model, and its roles in different stages are different. Key words: Neuropathic pain; Transient receptor potential cation channel subfamily A member 1; Dorsal root ganglion