2026-06-14T03:37:44Zhttps://repisalud.isciii.es/rest/oai/requestoai:repisalud.isciii.es:20.500.12105/170992024-11-28T14:42:42Zcom_20.500.12105_15322com_20.500.12105_2051col_20.500.12105_16927
Repisalud
author
Rivera, Patricia
author
Blanco, Eduardo
author
Bindila, Laura
author
Alen, Francisco
author
Vargas, Antonio
author
Rubio, Leticia
author
Pavón, Francisco-Javier
author
Serrano, Antonia
author
Lutz, Beat
author
Rodríguez de Fonseca, Fernando
author
Suárez, Juan
authoraffiliation
[Rivera,P; Blanco,E; Alen,F; Vargas,A; Pavón,FJ; Serrano,A; Rodríguez de Fonseca,F; Suárez,J[ UGC Salud Mental, Instituto de Investigación Biomédica de Málaga, Universidad de Málaga-Hospital Universitario Regional de Málaga, Málaga, Spain. [Blanco,E] Departament de Pedagogia i Psicologia, Facultat de Ciències de l'Educació, Universitat de Lleida, Lleida, Spain. [Bindila,L; Lutz,B] Institute of Physiological Chemistry, University Medical Center of the Johannes Gutenberg-University of Mainz, Mainz, Germany. [Rubio,L] Departamento de Anatomía y Medicina Legal, Universidad de Málaga, Málaga, Spain.
2024-01-15T18:17:46Z
2024-01-15T18:17:46Z
2015-09-29
10.3389/fncel.2015.00379
1662-5102
Frontiers in Cellular Neuroscience
http://hdl.handle.net/10668/2339
26483633
http://hdl.handle.net/20.500.12105/17099
Chronic alcohol exposure reduces endocannabinoid activity and disrupts adult neurogenesis in rodents, which results in structural and functional alterations. Cannabinoid receptor agonists promote adult neural progenitor cell (NPC) proliferation. We evaluated the protective effects of the selective CB1 receptor agonist ACEA, the selective CB2 receptor agonist JWH133 and the fatty-acid amide-hydrolase (FAAH) inhibitor URB597, which enhances endocannabinoid receptor activity, on NPC proliferation in rats with forced consumption of ethanol (10%) or sucrose liquid diets for 2 weeks. We performed immunohistochemical and stereological analyses of cells expressing the mitotic phosphorylation of histone-3 (phospho-H3+) and the replicating cell DNA marker 5-bromo-2'-deoxyuridine (BrdU+) in the main neurogenic zones of adult brain: subgranular zone of dentate gyrus (SGZ), subventricular zone of lateral ventricles (SVZ) and hypothalamus. Animals were allowed ad libitum ethanol intake (7.3 ± 1.1 g/kg/day) after a controlled isocaloric pair-feeding period of sucrose and alcoholic diets. Alcohol intake reduced the number of BrdU+ cells in SGZ, SVZ, and hypothalamus. The treatments (URB597, ACEA, JWH133) exerted a differential increase in alcohol consumption over time, but JWH133 specifically counteracted the deleterious effect of ethanol on NPC proliferation in the SVZ and SGZ, and ACEA reversed this effect in the SGZ only. JWH133 also induced an increased number of BrdU+ cells expressing neuron-specific β3-tubulin in the SVZ and SGZ. These results indicated that the specific activation of CB2 receptors rescued alcohol-induced impaired NPC proliferation, which is a potential clinical interest for the risk of neural damage in alcohol dependence.
eng
Alcohol
ACEA
JWH133
CB1 receptor
Neurogenesis
CB2 receptor
Consumo de alcohol
Alcoholismo
Benzamidas
bromodesoxiuridina
Carbamatos
Giro dentado
Dieta
Endocannabinoides
Etanol
marcadores genéticos
Histonas
Hidrolasas
Hipotálamo
Ventrículos laterales
Células madre nerviosas
Neuronas
Fosforilación
Ratas
Receptor cannabinoide CB1
Sacarosa
Tubulina (proteína)
Pharmacological activation of CB2 receptors counteracts the deleterious effect of ethanol on cell proliferation in the main neurogenic zones of the adult rat brain.
research article