1. ¹Department of Molecular and Cellular Neuroscience, Nencki Institute of Experimental Biology, Warsaw, Poland
2. ²Department of Pharmacology, Institute of Psychiatry and Neurology, Warsaw, Poland

Correspondence: Dr L Kaczmarek, Laboratory of Molecular Neurobiology, Nencki Institute, Pasteura 3 St, 02-093 Warsaw, Poland. Tel: +48 22 659 30 01; Fax: +48 22 822 53 42; E-mail: leszek@nencki.gov.pl

Received 10 April 2007; Revised 10 August 2007; Accepted 11 August 2007; Published online 12 September 2007.

Abstract

Alcohol-related cues may induce relapse to heavy alcohol drinking and promote molecular adaptations in discrete brain regions. An exact nature of these molecular alterations is still unknown. In the present study, rats trained to self-administer ethanol were tested for cue-induced reinstatement of ethanol seeking after 30 days of abstinence. Next, a detailed immunocytochemical analysis of c-Fos activation was performed within seven nuclei of the amygdala. In the second experiment, c-Fos activation after reinstatement of ethanol seeking induced by discrete cues was compared with the activation pattern of its putative partner (c-Jun) and regulators (extracellular signal-regulated kinases and c-Jun N-terminal kinases). Reexposure to ethanol-associated context cues (an extinction session) potentiated c-Fos expression within the basolateral and central amygdala. Repeated presentation of ethanol-associated discrete cues in an extinction/reinstatement session led to even stronger c-Fos activation in the latter nuclei. In the second experiment, reexposure to the ethanol-associated context and discrete cues activated both c-Jun and extracellular signal-regulated kinases (ERK1/2) in the basolateral amygdala. Our observations suggest that the basolateral and central amygdala may be specifically involved in alcohol-seeking behavior induced by discrete cues.