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. 2018 Apr 2;115(16):4282–4287. doi: 10.1073/pnas.1707047115

Fig. 1.

Fig. 1.

The AMPK activator AICAR eliminates anxiety-like behaviors following nicotine withdrawal. (A and B) Nicotine causes activation of the AMPK pathway in the hippocampus, as indicated by representative Western blot analyses of AMPK and pAMPK (n = 9) and ACC and pACC tissue (n = 3). *P < 0.05; ***P < 0.001. (C–E) Chronic AICAR administration increases pAMPK level in the hippocampus and reduces anxiety-like behavior at 24 h after cessation of nicotine. (C) Systemic AICAR treatment results in significant activation of the AMPK pathway in the hippocampus, indicating that the drug crosses the blood-brain barrier (n = 4; P < 0.05). (D and E) Anxiety-like behavior precipitated by nicotine withdrawal is reduced by AICAR. (D) NIH was tested at 24 h after nicotine withdrawal. AICAR before nicotine withdrawal prevented the increase in latency to feed observed in saline-treated mice undergoing 24-h withdrawal. Bars represent mean latency ± SEM (n = 7–13). *P < 0.05; **P < 0.01. (E) The MB test was performed at 48 h after nicotine withdrawal. Data represent the mean ± SEM number of marbles buried over 15 min (n = 7–8). **P < 0.01.