Fig. 6: l-CDL antagonizes spinal D2DR to attenuate morphine tolerance in mice through PI3K/Akt-MAPK signaling in a MOR-dependent manner. | Experimental & Molecular Medicine

Fig. 6: l-CDL antagonizes spinal D2DR to attenuate morphine tolerance in mice through PI3K/Akt-MAPK signaling in a MOR-dependent manner.

From: Selective blockade of spinal D2DR by levo-corydalmine attenuates morphine tolerance via suppressing PI3K/Akt-MAPK signaling in a MOR-dependent manner

Fig. 6

a–c Western blots showing increased levels of p-ERK1/2, p-p38, and p-JNK in the spinal cord after chronic morphine treatment, changes that were significantly decreased by the intrathecal administration of l-CDL. d–f Mice receiving a spinal D2DR siRNA injection with a morphine infusion showed a significant reduction in the levels of p-ERK1/2, p-p38, and p-JNK in the spinal cord. g–i Inhibition of spinal PI3K with its inhibitor LY 294002 also decreased the levels of p-ERK1/2, p-p38, and p-JNK in the spinal cord. j–l Intrathecal administration of the MOR antagonist CTOP (1 ng/10 μl) reversed the increased levels of p-ERK1/2, p-p38, and p-JNK in the spinal cord. Representative western blot bands and a summary of the data are shown. All spinal cords were collected on day 7, 30 min after chronic morphine exposure. Data are presented as means ± SE. n = 4, #P < 0.05, ##P < 0.01, compared with the control group; *P < 0.05, **P < 0.01, compared with the morphine group

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