RT Journal Article
T1 Pharmacological blockade of the fatty acid amide hydrolase (FAAH) alters neural proliferation, apoptosis and gliosis in the rat hippocampus, hypothalamus and striatum in a negative energy context.
A1 Rivera, Patricia
A1 Bindila, Laura
A1 Pastor, Antoni
A1 Pérez-Martín, Margarita
A1 Pavón, Francisco J
A1 Serrano, Antonia
A1 de la Torre, Rafael
A1 Lutz, Beat
A1 Rodríguez de Fonseca, Fernando
A1 Suárez, Juan
K1 URB597
K1 FAAH
K1 Cannabinoids
K1 Energy metabolism
K1 Neurogenesis
K1 Gliosis
K1 Bromodesoxiuridina
K1 Cannabinoides
K1 Carbamatos
K1 Caspasa 3
K1 Muerte celular
K1 Proliferación celular
K1 Colesterol
K1 Endocannabinoides
K1 Etanolaminas
K1 Glucosa
K1 Hipocampo
K1 Hipotálamo
K1 Microglía
K1 Ácidos oléicos
K1 Ácidos palmíticos
K1 Ratas
K1 Receptor cannabinoide CB1
K1 Triglicéridos
K1 Amidohidrolasas
K1 Apoptosis
K1 Astrocitos
K1 Benzamidas
K1 Peso corporal
K1 Cerebro
AB Endocannabinoids participate in the control of neurogenesis, neural cell death and gliosis. The pharmacological effect of the fatty acid amide hydrolase (FAAH) inhibitor URB597, which limits the endocannabinoid degradation, was investigated in the present study. Cell proliferation (phospho-H3(+) or BrdU(+) cells) of the main adult neurogenic zones as well as apoptosis (cleaved caspase-3(+)), astroglia (GFAP(+)), and microglia (Iba1(+) cells) were analyzed in the hippocampus, hypothalamus and striatum of rats intraperitoneally treated with URB597 (0.3 mg/kg/day) at one dose/4-days resting or 5 doses (1 dose/day). Repeated URB597 treatment increased the plasma levels of the N-acylethanolamines oleoylethanolamide, palmitoylethanolamide and arachidonoylethanolamine, reduced the plasma levels of glucose, triglycerides and cholesterol, and induced a transitory body weight decrease. The hippocampi of repeated URB597-treated rats showed a reduced number of phospho-H3(+) and BrdU(+) subgranular cells as well as GFAP(+), Iba1(+) and cleaved caspase-3(+) cells, which was accompanied with decreased hippocampal expression of the cannabinoid CB1 receptor gene Cnr1 and Faah. In the hypothalami of these rats, the number of phospho-H3(+), GFAP(+) and 3-weeks-old BrdU(+) cells was specifically decreased. The reduced striatal expression of CB1 receptor in repeated URB597-treated rats was only associated with a reduced apoptosis. In contrast, the striatum of acute URB597-treated rats showed an increased number of subventricular proliferative, astroglial and apoptotic cells, which was accompanied with increased Faah expression. Main results indicated that FAAH inhibitor URB597 decreased neural proliferation, glia and apoptosis in a brain region-dependent manner, which were coupled to local changes in Faah and/or Cnr1 expression and a negative energy context.
PB Frontiers Media
YR 2015
FD 2015-03-27
LK http://hdl.handle.net/10668/2340
UL http://hdl.handle.net/10668/2340
LA en
NO Rivera P, Bindila L, Pastor A, Pérez-Martín M, Pavón FJ, Serrano A, et al. Pharmacological blockade of the fatty acid amide hydrolase (FAAH) alters neural proliferation, apoptosis and gliosis in the rat hippocampus, hypothalamus and striatum in a negative energy context. Front Cell Neurosci. 2015; 9:98
NO Journal Article;
DS RISalud
RD Apr 8, 2025