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. 2011 Jun;163(4):857–875. doi: 10.1111/j.1476-5381.2011.01287.x

Figure 6.

Figure 6

Morphine withdrawal-induced cAMP-response element binding protein (CREB) activation in the hypothalamic paraventricular nucleus (PVN) is protein kinase C dependent. (A,C) Quantitative analysis and representative immunoblots of pCREB in the PVN tissue isolated from placebo or morphine-dependent rats concomitantly treated with calphostin C, chelerythrine or vehicle, 60 min after administration of naloxone. (B,D) Quantitative analysis and representative immunoblots of pERK1/2 expressions in the PVN 60 min after naloxone injection to morphine-dependent rats pretreated with vehicle, calphostin C or chelerythrine. Post hoc analysis revealed that the increase in CREB phosphorylation during morphine withdrawal was attenuated by both calphostin C and chelerythrine, whereas both ERK1 and ERK2 phosphorylation was attenuated by calphostin C (B) but not by chelerythrine (D). Each bar represents mean ± SEM (% of controls). *P < 0.05, **P < 0.01 versus placebo + vehicle + naloxone; +P < 0.05, ++P < 0.01, +++P < 0.001 versus morphine + vehicle + naloxone. chel, chelerythrine; cp, calphostin C; m, morphine pellets; n, naloxone; p, placebo pellets; veh, vehicle.