Jose Antonio López-Moreno1, Miguel Marcos2, Javier Calleja-Conde1, Victor Echeverry-Alzate1, Kora M Bühler1, Pilar Costa-Alba3, Edgar Bernardo4, Francisco-Javier Laso2, Fernando Rodríguez de Fonseca5, Roser Nadal6, Maria Paz Viveros7, Rafael Maldonado8, Elena Giné9. 1. Department of Psychobiology, School of Psychology, Complutense University of Madrid, Madrid, Spain. 2. Alcoholism Unit, Department of Internal Medicine, University Hospital of Salamanca, Salamanca, Spain. 3. Emergency Department, University Hospital of Salamanca, Salamanca, Spain. 4. Department of Vascular Biology and Inflammation, Fundación Centro Nacional de Investigaciones Cardiovasculares Carlos III, Madrid, Spain. 5. Fundación IMABIS, Laboratorio de Medicina Regenerativa, Hospital Regional Universitario Carlos Haya, Málaga, Spain. 6. Psychobiology Unit, School of Psychology, Institut de Neurociències, Universitat Autònoma de Barcelona, Barcelona, Spain. 7. Department of Physiology (Animal Physiology II), School of Biology, Complutense University of Madrid, Madrid, Spain. 8. Laboratori de Neurofarmacologia, Departament de Ciències Experimentals i de la Salut, Universitat Pompeu Fabra, Barcelona, Spain. 9. Department of Cellular Biology, School of Medicine, Complutense University of Madrid, Madrid, Spain.
Abstract
BACKGROUND: Alcohol binge drinking is one of the most common patterns of excessive alcohol use and recent data would suggest that histone deacetylases (HDACs) gene expression profiling could be useful as a biomarker for psychiatric disorders. METHODS: This study aimed to characterize the gene expression patterns of Hdac 1-11 in samples of rat peripheral blood, liver, heart, prefrontal cortex, and amygdala following repeated binge alcohol consumption and to determine the parallelism of Hdac gene expression between rats and humans in peripheral blood. To accomplish this goal, we examined Hdac gene expression following 1, 4, or 8 alcohol binges (3 g/kg, orally) in the rat, in patients who were admitted to the hospital emergency department for acute alcohol intoxication, and in rats trained in daily operant alcohol self-administration. RESULTS: We primarily found that acute alcohol binging reduced gene expression (Hdac1-10) in the peripheral blood of alcohol-naïve rats and that this effect was attenuated following repeated alcohol binges. There was also a reduction of Hdac gene expression in the liver (Hdac2,4,5), whereas there was increased expression in the heart (Hdac1,7,8) and amygdala (Hdac1,2,5). Additionally, increased blood alcohol concentrations were measured in rat blood at 1 to 4 hours following repeated alcohol binging, and the only group that developed hepatic steotosis (fatty liver) were those animals exposed to 8 alcohol binge events. Finally, both binge consumption of alcohol in humans and daily operant alcohol self-administration in rats increased Hdac gene expression in peripheral blood. CONCLUSIONS: Our results suggest that increases in HDAC gene expression within the peripheral blood are associated with chronic alcohol consumption, whereas HDAC gene expression is reduced following initial exposure to alcohol.
BACKGROUND:Alcohol binge drinking is one of the most common patterns of excessive alcohol use and recent data would suggest that histone deacetylases (HDACs) gene expression profiling could be useful as a biomarker for psychiatric disorders. METHODS: This study aimed to characterize the gene expression patterns of Hdac 1-11 in samples of rat peripheral blood, liver, heart, prefrontal cortex, and amygdala following repeated binge alcohol consumption and to determine the parallelism of Hdac gene expression between rats and humans in peripheral blood. To accomplish this goal, we examined Hdac gene expression following 1, 4, or 8 alcohol binges (3 g/kg, orally) in the rat, in patients who were admitted to the hospital emergency department for acute alcohol intoxication, and in rats trained in daily operant alcohol self-administration. RESULTS: We primarily found that acute alcohol binging reduced gene expression (Hdac1-10) in the peripheral blood of alcohol-naïve rats and that this effect was attenuated following repeated alcohol binges. There was also a reduction of Hdac gene expression in the liver (Hdac2,4,5), whereas there was increased expression in the heart (Hdac1,7,8) and amygdala (Hdac1,2,5). Additionally, increased blood alcohol concentrations were measured in rat blood at 1 to 4 hours following repeated alcohol binging, and the only group that developed hepatic steotosis (fatty liver) were those animals exposed to 8 alcohol binge events. Finally, both binge consumption of alcohol in humans and daily operant alcohol self-administration in rats increased Hdac gene expression in peripheral blood. CONCLUSIONS: Our results suggest that increases in HDAC gene expression within the peripheral blood are associated with chronic alcohol consumption, whereas HDAC gene expression is reduced following initial exposure to alcohol.
Authors: Gail A Cresci; Bryan Glueck; Megan R McMullen; Wei Xin; Daniella Allende; Laura E Nagy Journal: J Gastroenterol Hepatol Date: 2017-09 Impact factor: 4.029
Authors: John Peyton Bohnsack; Benjamin A Hughes; Todd K O'Buckley; Kamyra Edokpolor; Joyce Besheer; A Leslie Morrow Journal: Neuropsychopharmacology Date: 2018-02-27 Impact factor: 7.853
Authors: V Echeverry-Alzate; K M Bühler; J Calleja-Conde; E Huertas; R Maldonado; F Rodríguez de Fonseca; C Santiago; F Gómez-Gallego; A Santos; E Giné; J A López-Moreno Journal: Psychopharmacology (Berl) Date: 2018-11-23 Impact factor: 4.530
Authors: Javier Calleja-Conde; Victor Echeverry-Alzate; Elena Giné; Kora-Mareen Bühler; Roser Nadal; Rafael Maldonado; Fernando Rodríguez de Fonseca; Antoni Gual; Jose Antonio López-Moreno Journal: Br J Pharmacol Date: 2016-07-18 Impact factor: 8.739