The first two authors contributed equally to this study.
Ethanol-Induced Memory Impairment in a Discriminative Avoidance Task is State-Dependent
Version of Record online: 24 JUL 2012
Copyright © 2012 by the Research Society on Alcoholism
Alcoholism: Clinical and Experimental Research
Volume 37, Issue Supplement s1, pages E30–E39, January 2013
How to Cite
Sanday, L., Patti, C. L., Zanin, K. A., Fernandes-Santos, L., Oliveira, L. C., Kameda, S. R., Tufik, S. and Frussa-Filho, R. (2013), Ethanol-Induced Memory Impairment in a Discriminative Avoidance Task is State-Dependent. Alcoholism: Clinical and Experimental Research, 37: E30–E39. doi: 10.1111/j.1530-0277.2012.01905.x
- Issue online: 15 JAN 2013
- Version of Record online: 24 JUL 2012
- Manuscript Accepted: 6 JUN 2012
- Manuscript Received: 26 AUG 2011
- Fundação de Amparo a Pesquisa do Estado de São Paulo. Grant Numbers: 1998/14303-3, 2009/00465-9, 2008/08823-8
- Conselho Nacional de Desenvolvimento Científico e Tecnológico
- Fundação Coordenação de Aperfeiçoamento de Pessoal de Nível Superior
- Associação Fundo de Incentivo à Pesquisa
- Plus-Maze Discriminative Avoidance Task
A considerable amount of experimental evidence has demonstrated ethanol (EtOH) induced amnestic effects following EtOH administration during pretraining in a variety of tasks both in humans and in laboratory animals. Although the phenomenon of state-dependency is known to play a critical role in memory deficits induced by both pharmacological and nonpharmacological pretraining perturbations, the involvement of this phenomenon in EtOH-induced anterograde amnesia has been overlooked. This study aimed to investigate the role of state-dependency in EtOH-induced amnestic effects and its interactions with the well-known anxiolysis and locomotor alterations.
Mice were treated with 1.2 or 2.4 g/kg EtOH before training and/or before testing in the plus-maze discriminative avoidance task, an animal model that concomitantly evaluates learning, memory, anxiety-like behavior, and general activity.
Whereas both doses of EtOH induced anxiolysis, the 1.2 g/kg dose enhanced locomotion while the 2.4 g/kg dose decreased it. In addition, the administration of 1.2 g/kg of this drug during pretraining caused memory impairment, which was counteracted by the pretest administration of the same dose, revealing the participation of the state-dependency. Conversely, the administration of 2.4 g/kg EtOH led to amnestic effects irrespective of the time of the administration (pretraining and/or pretest), eliminating the influence of state-dependency.
Our data demonstrate that EtOH-induced memory deficits are critically related to state-dependency, which can also be affected by the dose range. These results indicate the possible participation of EtOH-induced modifications in anxiety and motor activity levels in relation to state-dependent memory deficits.