Figure 7

Initiation of IGF-1R/Fyn signaling by MOR in the traumatic mice. MOR (+/−) and MOR (−/−) mice were subjected to surgical trauma, some of these mice were injected icv with IGF-1. Thus, 5 groups of mice were created: Con, T1, T1 + IGF-1, T3, T3 + IGF-1 (n = 5 for each group). Synaptoneurosome in the frontal cortex was prepared and pooled with anti-Fyn antibody, ³²P incorporation were determined by incubating with 5 μg of Src substrate peptide in kinase buffer at 30°C. Data was converted to pmol/min (A). Synaptoneurosome was prepared and assayed for association of IGF-1R and Fyn by immunoprecipitation. Anti-Fyn was used as immunoprecipitate antibody and anti-IGF-1R as immuno blot antibody (B). Panel C depicts quantitative analysis of B. Cortical neurons from MOR (+/−) and MOR (−/−) mice were cultured for 10 days, then exposed to IL-1β and IL-1ra respectively, association of IGF-1R and Fyn was determined by immunoprecipitation (D). Panel E depicts quantitative analysis of D. MOR (+/−) and MOR (−/−) mice were subjected to surgical trauma, some of these mice were injected icv with IGF-1. Thus, 5 groups of mice were created: Con, T1, T1 + IGF-1, T3, T3 + IGF-1 (n = 5 for each group). Homogenates of spleen were prepared, and lymphocyte proliferation (F) and NK cell activity (G) were assayed by [³ H] incorporation. Data were normalized and calculated as percentage of control, each value represents mean±SD for 3 independent experiments. p < 0.05, *vs Con, ^#vs traumatized. Con: control; T1 and 3: 1 and 3 days after trauma.