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

Figure 9.

Figure 9

Activation of the hypothalamic-pituitary-adrenocortical axis during morphine withdrawal is attenuated by PKC inhibition. Placebo or morphine-dependent rats were pretreated with dimethyl sulphoxide (DMSO), SL-327, calphostin C or chelerythrine and plasma levels of corticosterone (a marker of hypothalamic-pituitary-adrenocortical axis activity) were determined 60 min after naloxone injection. Each bar represents mean ± SEM. Post hoc analysis revealed a significant increase in plasma corticosterone concentration after naloxone-induced morphine withdrawal, which was attenuated in calphostin C-pretreated rats (B) and chelerythrine-pretreated rats (C) but not in SL-327-pretreated rats. (A) **P < 0.01 versus placebo + DMSO + naloxone; &P < 0.05 versus placebo + DMSO + naloxone. (B) ***P < 0.001 versus placebo + vehicle + naloxone; +P < 0.05 versus morphine + vehicle + naloxone; ###P < 0.001 versus placebo + calphostin C + naloxone. (C) ***P < 0.001 versus placebo + vehicle + naloxone; ++P < 0.01 versus morphine + vehicle + naloxone; ###P < 0.001 versus placebo + chelerythrine + naloxone. chel, chelerythrine; cp, calphostin C; m, morphine pellets; n, naloxone; p, placebo pellets.