Figure 2. Morphine withdrawal-induced CREB activation in the PVN is dependent on α₁-adrenoceptor stimulation.

Quantitative analysis and representative immunoblots (A) of pCREB in the PVN tissue isolated from placebo or morphine-dependent rats pretreated with prazosin 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 blocked by prazosin (1 mg/kg i.p.). Each bar represents mean ± SEM (% of controls); p: placebo pellets; m: morphine pellets; veh: vehicle; n: naloxone; praz: prazosin. **p<0.01 vs control pellets (placebo)+vehicle+naloxone; ⁺⁺⁺p<0.001 vs. morphine-treated rats+ to control and to morphine-dependent rats. vehicle+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 prazosin 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 a significant decrease in pCREB immunoreactivity in prazosin-pretreated rats. *p<0.05 versus morphine+vehicle+naloxone.