RT Journal Article
T1 Pharmacological activation of CB2 receptors counteracts the deleterious effect of ethanol on cell proliferation in the main neurogenic zones of the adult rat brain.
A1 Rivera, Patricia
A1 Blanco, Eduardo
A1 Bindila, Laura
A1 Alen, Francisco
A1 Vargas, Antonio
A1 Rubio, Leticia
A1 Pavón, Francisco J
A1 Serrano, Antonia
A1 Lutz, Beat
A1 Rodríguez de Fonseca, Fernando
A1 Suárez, Juan
K1 Alcohol
K1 ACEA
K1 JWH133
K1 CB1 receptor
K1 Neurogenesis
K1 CB2 receptor
K1 Consumo de alcohol
K1 Alcoholismo
K1 Benzamidas
K1 bromodesoxiuridina
K1 Carbamatos
K1 Giro dentado
K1 Dieta
K1 Endocannabinoides
K1 Etanol
K1 marcadores genéticos
K1 Histonas
K1 Hidrolasas
K1 Hipotálamo
K1 Ventrículos laterales
K1 Células madre nerviosas
K1 Neuronas
K1 Fosforilación
K1 Ratas
K1 Receptor cannabinoide CB1
K1 Sacarosa
K1 Tubulina (proteína)
AB 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.
PB Frontiers Media
YR 2015
FD 2015-09-29
LK http://hdl.handle.net/10668/2339
UL http://hdl.handle.net/10668/2339
LA en
NO Rivera P, Blanco E, Bindila L, Alen F, Vargas A, Rubio L, et al. Pharmacological activation of CB2 receptors counteracts the deleterious effect of ethanol on cell proliferation in the main neurogenic zones of the adult rat brain. Front Cell Neurosci. 2015; 9:379
NO Journal Article;
DS RISalud
RD Apr 7, 2025