Deficits in amygdaloid cAMP-responsive element–binding protein signaling play a role in genetic predisposition to anxiety and alcoholism
J. Clin. Invest. Subhash C. Pandey, et al. 115:2762 doi:10.1172/JCI24381 [Go to this article.]

Figure 2
Voluntary ethanol intake and CREB signaling in the amygdala of P and NP rats. (A) Low-magnification views of CREB, p-CREB, and PKA-Cα gold immunolabeling in CeA structures of P and NP rats with or without ethanol exposure. Photomicrographs show CREB-positive nuclei (upper panels), p-CREB–positive nuclei (middle panels), and PKA-Cα–positive cell bodies (lower panels) in the CeA of NP and P rats with or without ethanol exposure. Insets show the immuno-gold particles within a single nucleus (CREB and p-CREB) or cell body (PKA-Cα) at high magnification (×100). Scale bar: 40 μm. (B) Effect of voluntary ethanol intake on CREB, p-CREB, and PKA-Cα protein levels in various amygdaloid structures (CeA, MeA, and BLA) of P and NP rats. Values represent the mean ± SEM of 4–6 rats in each group. *P < 0.001 versus respective controls.