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. Author manuscript; available in PMC: 2016 Dec 1.
Published in final edited form as: Alcohol. 2015 Oct 23;49(8):773–779. doi: 10.1016/j.alcohol.2015.09.001

Fig. 1.

Fig. 1

Cellular mechanisms that mediate alterations in mPFC synchrony and cognitive disruption following chronic ethanol exposure. Under control conditions (left panel), synchronous activation of appropriate cortical networks mediates cognitive control over behavior. At the cellular level this is achieved via dopamine modulation of intrinsic and synaptic currents within pyramidal neurons (green) and FSINs (red) to promote temporal and spatial precision over networks to increase specificity of information flow by synchronizing specific groups of neurons (symbolized by bold lines). Following chronic alcohol exposure (right panel), network synchrony is disrupted due to the reduction in D2/D4 receptor modulation of excitability of pyramidal neurons and FSINs. The loss of D2/D4 receptor-mediated recruitment of FSINs (lighter red color) results in desynchronization of pyramidal networks and loss of specificity over information flow (all pyramidal cells in bold green).