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Sleep supports the consolidation of memory, and it has been proposed that this enhancing effect of sleep pertains in particular to memories which are encoded under control of prefrontal–hippocampal circuitry into an episodic memory system. Furthermore, repeated reactivation and transformation of such memories during sleep are thought to promote the de-contextualization of these memories. Here, we aimed to establish a behavioral model for the study of such sleep-dependent system consolidation in rats, using a go/nogo conditional discrimination learning task known to essentially depend on prefrontal–hippocampal function. Different groups of rats were trained to criterion on this task and, then, subjected to 80-min retention intervals filled with spontaneous morning sleep, sleep deprivation, or spontaneous evening wakefulness. In a subsequent test phase, the speed of relearning of the discrimination task was examined as indicator of memory, whereby rats were either tested in the same context as during training or in a different context. Sleep promoted relearning of the conditional discrimination task, and this effect was similar for testing memory in the same or different context (p < 0.001). Independent of sleep and wakefulness during the retention interval, animals showed faster relearning when tested in the same context as during learning, compared with testing in a different context (p < 0.001). The benefitting effect of sleep on discrimination learning was primarily due to an enhancing effect on response suppression during the nogo stimulus. We infer from these results that sleep enhances memory for inhibitory behavioral control in a generalized context-independent manner and thereby might eventually also contribute to the abstraction of schema-like representations.

Marion Inostroza por su colaboración en la ejecución del experimento.Contacto: G. Miguez, State University of New York at Binghamton, Binghamton, NY, 13902-6000, United States of America. gmiguez1@binghamton.edu ResumenEn esta investigación se estudió la reinstauración de la tolerancia al efecto atáxico del etanol en tres grupos de ratas. Para todos los sujetos un estímulo visual (i.e., estímulo condicionado; EC) fue pareado en repetidas ocasiones con el efecto de una dosis de etanol (i.e., estímulo incondicionado, EI). Luego, los sujetos recibieron ensayos no pareados del EC con el fin de extinguir la asociación EC-EI formada en la fase previa. Posterior a la extinción, un grupo recibió una presentación no pareada del EI en el contexto de extinción, un segundo grupo recibió una presentación no pareada del EI en un contexto novedoso, y el tercer grupo no recibió presentaciones del EI. Finalmente, se evaluó la respuesta de tolerancia al efecto atáxico del etanol en ensayos de readquisición. Los datos obtenidos demuestran que la administración no señalada del efecto del etanol en el organismo reinstaura la respuesta de tolerancia anteriormente extinguida, y que el contexto donde se realiza la administración influye en la magnitud de la reinstauración de la respuesta condicionada de tolerancia. Estos datos, juntos con otros de experimentos previos, arrojan luces sobre los mecanismos que producen recaídas en terapias de exposición a claves.Palabras clave: alcohol, adicción, condicionamiento Pavloviano, tolerancia a las drogas, reinstauración. AbstractThe reinstatement of the ataxic effect of ethanol was studied in three groups of rats. All subjects received a visual stimulus (i.e., conditioned stimulus, CS), paired in repeated occasions with the effect of an ethanol dose (i.e., unconditioned stimulus, US). Then, all subjects received unpaired presentations of the CS aimed at extinguishing the CS-US association formed in the previous phase. After extinction, one group received an unpaired presentation of the US in the extinction context, a second group received an unpaired presentation of the US in a new context, and a third group did not receive US presentations. Finally, the tolerance response to the ataxic effect of ethanol was assessed in reacquisition trials. The results show that a nonsignaled administration of ethanol is efficient in reinstating an extinguished tolerance response, and that the context in which the ethanol is administered determines the magnitude of the reinstated conditioned response. This study, together with previous data, helps to understand the mechanisms of relapse in cue exposure therapies.

En 2 experimentos se investigó el rol de las claves de extinción (CE), y estímulos asociados a estas, en la readquisición de la tolerancia condicionada al etanol. La ataxia causada por el etanol fue medida en 80 ratas, utilizando planos de deslizamiento en un procedimiento de 5 fases. El primer experimento (que utilizó 4 contextos y 40 ratas) mostró que la presentación del contexto de extinción por sí solo disminuyó la efectividad de la CE para reducir la readquisición de respuesta. El segundo experimento (hecho en un solo contexto, con 40 ratas y con la diferencia de que se usaron 2 estímulos que fueron pareados para algunos sujetos o explícitamente no pareados para otros) mostró que una clave secundaria puede reducir la readquisición, independientemente de si fue pareada con la CE o no. Los resultados de análisis de varianza mixtos y factoriales sugieren que la CE afectaría la recuperación de la respuesta a través de una asociación con el contexto de extinción; sin embargo, una clave de segundo orden, asociada a la CE, no lograría activar dicha asociación. Palabras clave: extinción, condicionamiento clásico, tolerancia a las drogas, etanol, ataxia Two experiments analyzed the role of extinction cues (EC) and stimuli associated to them in the reacquisition of conditioned ethanol tolerance. Ethanol-induced ataxia was measured in 80 rat subjects using a tilting plane, in a 5-phase procedure. The first experiment (which used 4 contexts and 40 rats) showed that the presentation of the extinction context by itself diminished the effectiveness of ECs in reducing response reacquisition. The second experiment (conducted in a single context with 40 rats and using 2 stimulus paired for some subjects or explicitly unpaired for others) showed that a secondary cue can reduce reacquisition, regardless of whether it was paired with the EC or not. The results of mixed and factor analyses of variance suggest that ECs affect response recovery through an association with the extinction context; however, a second-order cue associated to an EC appears to be unable to activate this association.

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