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Figure 4 | Molecular Pain

Figure 4

From: Targeting adenosine monophosphate-activated protein kinase (AMPK) in preclinical models reveals a potential mechanism for the treatment of neuropathic pain

Figure 4

Treatment with AMPK activators suppresses translation regulation signaling. A) Treatment of mouse sensory neurons cultured in the presence of NGF (50 ng/ml) with metformin (2 and 20 mM) for 1 hour induces a dose-dependent increase in the phosphorylation of AMPK. Metformin treatment abrogates the phosphorylation of mTOR, 4EBP and rS6 in a dose-dependent manner. Metformin does not suppress the ERK-eIF4E pathway. B) AMPK allosteric activator A769662 suppresses translation regulation signaling. Treatment of mouse sensory neurons with A769662 (50 and 500 μM) results in a dose dependent suppression of phosphorylation of ERK, eIF4E, mTOR, 4EBP, AKT and rS6. C) Treatment of mouse sensory neurons with AICAR (0.5 and 2 mM) for 1 hour results in a dose dependent activation of AMPK. Moreover, AICAR dose-dependently suppresses the phosphorylation of ERK, eIF4E, AKT, TSC2, 4EBP and rS6. N = 6 per group. *p < 0.05, **p < 0.01 and ***p < 0.001.

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Molecular Pain

ISSN: 1744-8069

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