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. Author manuscript; available in PMC: 2022 Sep 1.
Published in final edited form as: Neuropharmacology. 2021 May 26;195:108623. doi: 10.1016/j.neuropharm.2021.108623

Figure 5.

Figure 5.

Molecular mechanism of CB1 receptor-mediated attenuation of alcohol drinking and anxiety-like behavior. The blockade of CB1 receptors with neutral CB1 antagonist AM4113 leads to an increase in cAMP mediated CREB phosphorylation as these receptors are negatively coupled to adenylate cyclase (AC) and increase the levels of CREB binding protein (CBP). Direct or indirect activation of CBP/CREB signaling increases CBP and histone acetylation globally and at the Npy gene specifically leading to increased NPY expression in the amygdala. This CB1 receptor-mediated modulation of NPY expression through epigenetic modification via histone acetylation may be one of the important molecular mechanisms in the amygdala underlying regulation of alcohol consumption and anxiety-like behavior. eCB, endocannabinoid; CB1, Cannabinoid Receptor 1; cAMP, Cyclic adenosine monophosphate; PKA, Protein kinase A; CREB, cAMP-response element binding protein; pCREB, phosphorylated CREB; CBP, CREB binding protein; CRE, cAMP response element site; NPY, Neuropeptide Y.