RESUMO
Objective To evaluate the role of spinal astrocytes in posttraumatic stress disorder (PTSD)-induced hyperalgesia in rats. Methods Forty pathogen-free healthy male Sprague-Dawley rats, aged 6-8 weeks,weighing 200-250 g, were divided into 4 groups(n=10 each)using a random number table:control group(group C), group PTSD, normal saline group(group NS)and fluorocitrate group (group FC).The rats were exposed to single prolonged stress for establishment of the PTSD model in PTSD, NS and FC groups. At 30 min before establishment of the model and 1-7 days after establishment of the model,normal saline 10 μl was intraperitoneally injected in group NS, and 1 nmol∕10 μl fluorocitrate 10 μl, an inhibitor of astrocyte activation, was intraperitoneally injected in group FC. The mechanical paw withdrawal threshold(MWT)was measured at 24 h before establishment of the model and on 1, 2, 3, 5 and 7 days after establishment of the model. Four rats were sacrificed after measurement of pain threshold on 1 and 7 days after establishment of the model, and the lumbar segment(L3-5)of the spinal cord was re-moved for determination of the expression of glial fibrillary acidic protein(GFAP, an astrocyte marker)u-sing Western blot. Results Compared with group C, the MWT was significantly decreased at each time point after establishment of the model,and the expression of spinal GFAP was up-regulated on 1 and 7 days after establishment of the model in PTSD,NS and FC groups(P<005). Compared with group PTSD, no significant change was found in the MWT at each time point in group NS(P>005),and the MWT was sig-nificantly increased at each time point after establishment of the model,and the expression of spinal GFAP was down-regulated on 1 and 7 days after establishment of the model in group FC(P<005).Conclusion Activation of spinal astrocytes is involved in PTSD-induced hyperalgesia in rats.