Figure 7.

Proposed model for Arc modulation of synaptic strengthening in the CeA during alcohol dependence. The present investigation revealed that increased BDNF→ trkB → Arc signaling in the CeA might be involved in increased synaptic strengthening (increased DSD) that may be operative in the anxiolytic effects of acute ethanol exposure in rats. Conversely, development of anxiety-like behaviors might be related to decreased BDNF → trkB → Arc signaling associated with decreased DSD in the CeA during ethanol withdrawal after chronic exposure. BDNF infusion into the CeA attenuated the anxiety-like behaviors and normalized the reduction in BDNF–Arc signaling during ethanol withdrawal. Arc antisense ODN infusion into the CeA decreased the DSD in the CeA, provoked anxiety-like behaviors, and promoted alcohol intake. Thus, BDNF–Arc signaling and its relationship to dendritic spines in the CeA is crucial in understanding the underpinning mechanisms of anxiety and alcoholism. MEK, Mitogen-activated protein kinase kinase.