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. Author manuscript; available in PMC: 2012 Dec 1.
Published in final edited form as: Neuropharmacology. 2010 Dec 31;61(7):1097–1108. doi: 10.1016/j.neuropharm.2010.12.028

Figure 1. Chronic ethanol exposure occludes distinct forms of long-term synaptic plasticity in the lateral/basolateral amygdala.

Figure 1

(A) The panels are reprinted from Biological Psychiatry (58), Stephens et al., “Repeated ethanol exposure and withdrawal impairs human fear conditioning and depresses long-term potentiation in rat amygdala and hippocampus”, 392–400, Copyright (2005), with permission from Elsevier. (Left) Representation of the horizontal slice preparation used in this study illustrates the relationships between the recording electrode (R), the stimulator (S), the lateral amygdala (LA), and anatomical boundaries like the external capsule. (Right) Theta burst stimulation (TBS) of the external capsule caused robust long-term potentiation of synaptic responses in slices prepared from control animals (M) while repeated withdrawal from a chronic exposure to an ethanol-containing liquid diet (F) reduced the magnitude of this form of plasticity. (B) Panels reprinted from Alcohol (43), Läck et al., “Chronic ethanol and withdrawal effects on kainate receptor-mediated excitatory neurotransmission in the rat basolateral amygdala”, 25–33, Copyright (2009), with permission from Elsevier. (Left) Sample fEPSP responses recorded in basolateral amygdala in control brain slices (CON) or 24hr after a chronic intermittent exposure to ethanol vapor (24WD). Kainate receptor-dependent long-term synaptic potentiation was initiated by a 15min exposure to the agonist ATPA ((RS)-2-Amino-3-(3-hydroxy-5-tert-butylisoxazol-4-yl) propanoic acid; 5 μM). (Right) The magnitude of ATPA-induced LTP was significantly depressed by chronic ethanol exposure (not shown) and withdrawal.