Your browser doesn't support javascript.
loading
Chronic voluntary alcohol consumption causes persistent cognitive deficits and cortical cell loss in a rodent model.
Charlton, Annai J; May, Carlos; Luikinga, Sophia J; Burrows, Emma L; Hyun Kim, Jee; Lawrence, Andrew J; Perry, Christina J.
Afiliación
  • Charlton AJ; Florey Department of Neuroscience and Mental Health, University of Melbourne, Parkville, VIC, 3052, Australia.
  • May C; Florey Department of Neuroscience and Mental Health, University of Melbourne, Parkville, VIC, 3052, Australia.
  • Luikinga SJ; Mental Health Theme, The Florey Institute of Neuroscience and Mental Health, Parkville, VIC, 3052, Australia.
  • Burrows EL; Florey Department of Neuroscience and Mental Health, University of Melbourne, Parkville, VIC, 3052, Australia.
  • Hyun Kim J; Mental Health Theme, The Florey Institute of Neuroscience and Mental Health, Parkville, VIC, 3052, Australia.
  • Lawrence AJ; Florey Department of Neuroscience and Mental Health, University of Melbourne, Parkville, VIC, 3052, Australia.
  • Perry CJ; Mental Health Theme, The Florey Institute of Neuroscience and Mental Health, Parkville, VIC, 3052, Australia.
Sci Rep ; 9(1): 18651, 2019 12 09.
Article en En | MEDLINE | ID: mdl-31819151
Chronic alcohol use is associated with cognitive decline that impedes behavioral change during rehabilitation. Despite this, addiction therapy does not address cognitive deficits, and there is poor understanding regarding the mechanisms that underlie this decline. We established a rodent model of chronic voluntary alcohol use to measure ensuing cognitive effects and underlying pathology. Rats had intermittent access to alcohol or an isocaloric solution in their home cage under voluntary 2-bottle choice conditions. In Experiments 1 and 2 cognition was assessed using operant touchscreen chambers. We examined performance in a visual discrimination and reversal task (Experiment 1), and a 5-choice serial reaction time task (Experiment 2). For Experiment 3, rats were perfused immediately after cessation of alcohol access period, and volume, cell density and microglial populations were assessed in the prefrontal cortex and striatum. Volume was assessed using the Cavalieri probe, while cell and microglial counts were estimated using unbiased stereology with an optical fractionator. Alcohol-exposed and control rats showed comparable acquisition of pairwise discrimination; however, performance was impaired when contingencies were reversed indicating reduced behavioral flexibility. When tested in a 5-choice serial reaction time task alcohol-exposed rats showed increased compulsivity and increased attentional bias towards a reward associated cue. Consistent with these changes, we observed decreased cell density in the prefrontal cortex. These findings confirm a detrimental effect of chronic alcohol and establish a model of alcohol-induced cognitive decline following long-term voluntary intake that may be used for future intervention studies.
Asunto(s)

Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Consumo de Bebidas Alcohólicas / Cognición / Alcoholismo / Disfunción Cognitiva Tipo de estudio: Etiology_studies / Prognostic_studies Límite: Animals / Humans Idioma: En Revista: Sci Rep Año: 2019 Tipo del documento: Article País de afiliación: Australia Pais de publicación: Reino Unido

Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Consumo de Bebidas Alcohólicas / Cognición / Alcoholismo / Disfunción Cognitiva Tipo de estudio: Etiology_studies / Prognostic_studies Límite: Animals / Humans Idioma: En Revista: Sci Rep Año: 2019 Tipo del documento: Article País de afiliación: Australia Pais de publicación: Reino Unido