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Fig. 1 | Molecular Pain

Fig. 1

From: Alleviating neuropathic pain mechanical allodynia by increasing Cdh1 in the anterior cingulate cortex

Fig. 1

SNI enhanced c-Fos and GluR1 AMPA receptors expression. A Mechanical withdrawal thresholds were measured in Sham and SNI rats before and 1, 3, 7, 14 days after surgery. Results are expressed as mean ± SD (n = 6, for each group); *p < 0.05 vs. Sham. B Representative rat section through the ACC, 1.7 mm rostral to the bregma. Photomicrographs of the black box (0.513 mm × 0.385 mm) used in C. C-Fos immunostaining in the ACC of rats 3, 7, and 14 days after nerve injury. Scale bar 100 μm. D C-Fos-positive cells were counted on both sides of the ACC using the black box shown in B (n = 3, two sections per rat). Results are expressed as mean ± SD (n = 3); *p < 0.05 vs. Sham. E Representative Western blotting showing the redistribution of AMPA receptor GluR1 subunits in the ACC after nerve injury. F In the ACC, total GluR1 subunit protein expression was unaffected by nerve injury. Results are expressed as mean ± SD (n = 3, each group); p > 0.05 vs. Sham. G GluR1 membrane expression in the ACC of Sham- and SNI-operated rats. GluR1 abundance in membrane fractions increased significantly 3 and 7 days after nerve injury (n = 3 per group). Error bars SD; *p < 0.05 vs. Sham control

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