Fig. 3
EphA4–APCCdh1-dependent signaling is involved in SNI-induced redistribution of AMPA receptor GluR1 subunit in ACC. A Representative Western blotting showing levels of total and cytosolic Cdh1 in the ACC. B, C Peripheral nerve injury significantly reduced total Cdh1 expression (B) and correspondingly increased cytosolic Cdh1 levels (C) in the ACC obtained between 3 and 14 days post-SNI (n = 3 per group). Error bars SD; *p < 0.05 vs. Sham control. D Fluorescence photomicrographs showing the change in Cdh1 intracellular location in the ACC after nerve injury. Sections were labelled with anti-Cdh1 (green) and nuclei stained with DAPI (blue). Cdh1 was highly expressed in nucleus (c), whereas in the SNI group, Cdh1 translocated from the nucleus to cytosol (f). Scale bar 50 μm. E, F Total and cytosolic Cdh1 levels in the hippocampus did not change 3 days after nerve injury. Results are expressed as mean ± SD (n = 3, each group); p > 0.05 vs. Sham. G Immunostaining shows EphA4 expression in the ACC of Sham-operated rats (a), and SNI rats at post-operative day 3 (b) and 7 (c). H Representative Western blotting of EphA4 expression in the ACC of Sham and SNI-operated rats. I EphA4 levels on day 3 and 7 after nerve injury were significantly lower in SNI-operated rats than in Sham-operated rats. Results are expressed as mean ± SD (n = 3, each group); *p < 0.05 vs. Sham. J EphA4 interacted with Cdh1, APC2, and GluR1 in the ACC of Sham- and SNI-operated rats. ACC homogenates (14 days after surgery) were immunoprecipitated with antibodies to EphA4, and immunoblotted with antibodies to Cdh1, APC2, GluR1, or EphA4