Figure 7. Pretreatment with DOR antagonist restores CXCR4 function in MOR−/− mice.

(a) MOR−/− mouse brain homogenates were exposed to CXCL12 or DOR agonist (SNC80)/antagonist (naltrindole) as indicated. The graph represents the mean ratio, ± SEM, of agonist-stimulated GTPγS incorporation over basal (n=3; F_{5, 66}= 9.2, *** P < 0.001; * P < 0.05 vs SNC80 alone); (b) WT mice (P9) were pretreated with saline or naltrindole acutely (acute: single injection, 1 mg/kg, subcutaneously) and killed after the indicated time. Brain slices were treated with SNC80 (1μM) and processed for [³⁵S]GTPγS autoradiography. Analysis was performed in the cortex and hippocampus; overall results are reported in the graphs. Data are expressed as mean ± SEM of three animals for experimental group (F_{3, 60}= 12.87, * P < 0.05 and ** P < 0.005 vs saline-treated WT mice); (c) MOR−/− mice (P9) were pretreated with saline or naltrindole acutely (acute: single injection, 1mg/kg, subcutaneously) and killed after the indicated time. Brain slices were treated with CXCL12 (50nM) and processed for [³⁵S]GTPγS autoradiography. Analysis was performed in the cortex and hippocampus and reported in the graphs. Data are expressed as mean ± SEM of three animals for experimental group (F_{3, 60}= 4.358, * P < 0.05 and ** P < 0.01 vs saline-treated).