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. 2012 Feb 15;7(2):e31119. doi: 10.1371/journal.pone.0031119

Figure 3. Morphine withdrawal-induced CREB activation in the PVN is not dependent on β-adrenoceptor stimulation.

Figure 3

Quantitative analysis and representative immunoblots (A) of pCREB in the PVN tissue isolated from placebo or morphine-dependent rats pretreated with propranolol before saline or naloxone injection to control and to morphine-dependent rats. Post hoc analysis revealed that the increase in CREB phosphorylation during morphine withdrawal was not modified by propranolol (3 mg/kg i.p.). Each bar represents mean ± SEM (% of controls); p: placebo pellets; m: morphine pellets; veh: vehicle; n: naloxone; prop: propranolol. **p<0.01 vs. control pellets (placebo)+naloxone; ++p<0.01 vs. placebo-treated rats+propranolol+naloxone. PVN was also processed for pCREB immunohistochemistry. (B, C) represents immunohistochemical detection of pCREB in the PVN from morphine-treated rats receiving vehicle and naloxone (B) or propranolol plus naloxone (C). 3V: third ventricle. Scale bar: 100 µm. D: quantitative analysis of pCREB immunoreactivity the PVN. Data correspond to mean ± SEM. Post hoc analysis revealed no significant effects of propranolol pretreatment on pCREB immunoreactivity.