RT Journal Article
T1 Perinatal asphyxia results in altered expression of the hippocampal acylethanolamide/endocannabinoid signaling system associated to memory impairments in postweaned rats.
A1 Blanco, Eduardo
A1 Galeano, Pablo
A1 Holubiec, Mariana I
A1 Romero, Juan I
A1 Logica, Tamara
A1 Rivera, Patricia
A1 Pavón, Francisco J
A1 Suarez, Juan
A1 Capani, Francisco
A1 Rodríguez de Fonseca, Fernando
K1 Perinatal asphyxia
K1 Hippocampus
K1 Memory
K1 DAGLα
K1 NAPE-PLD
K1 CB1
K1 PPARα
K1 FAAH
K1 Animales
K1 Asfixia
K1 Atención
K1 Baños
K1 Procesos bioquímicos
K1 Isquemia cerebral
K1 Cesárea
K1 Cognición
K1 Endocannabinoides
K1 Proteína ácida fibrilar de la glía
K1 Memoria
K1 Modelos animales
K1 Enfermedades del sistema nervioso
K1 Neurogénesis
K1 Plasticidad neural
K1 Ácidos oleicos
K1 Embarazo
K1 Procesos fisiológicos
K1 Ratas
AB Perinatal asphyxia (PA) is an obstetric complication that strongly affects the CNS. The endocannabinoid system (ECS) is a lipid transmitter system involved in several physiological processes including synaptic plasticity, neurogenesis, memory, and mood. Endocannabinoids, and other acylethanolamides (AEs) without endocannabinoid activity, have recently received growing attention due to their potential neuroprotective functions in neurological disorders, including cerebral ischemia. In the present study, we aimed to analyze the changes produced by PA in the major metabolic enzymes and receptors of the ECS/AEs in the hippocampus using a rodent model of PA. To induce PA, we removed uterine horns from ready-to-deliver rats and immersed them into a water bath during 19 min. Animals delivered spontaneously or by cesarean section were employed as controls. At 1 month of age, cognitive functions were assessed and immunohistochemical procedures were carried out to determine the expression of NeuN and glial fibrillary acidic protein, enzymes responsible for synthesis (DAGLα and NAPE-PLD) and degradation (FAAH) of ECS/AEs and their receptors (CB1 and PPARα) in the hippocampus. Postweaned asphyctic rats showed impaired recognition and spatial reference memory that were accompanied by hippocampal astrogliosis and changes in the expression of enzymes and receptors. The most remarkable findings in asphyctic rats were a decrease in the expression of NAPE-PLD and PPARα in both hippocampal areas CA1 and CA3. In addition, postweaned cesarean delivery rats showed an increase in the immunolabeling for FAAH in the hippocampal CA3 area. Since, NAPE-PLD and PPARα are proteins that participate in the biochemical process of AEs, specially the neuroprotective oleoylethanolamide, these results suggest that PA dysregulates this system. These data encourage conducting future studies using AEs as potential neuroprotective compounds in animal models of PA.
PB Frontiers Media
YR 2015
FD 2015-11-03
LK http://hdl.handle.net/10668/2338
UL http://hdl.handle.net/10668/2338
LA en
NO Blanco E, Galeano P, Holubiec MI, Romero JI, Logica T, Rivera P, et al. Perinatal asphyxia results in altered expression of the hippocampal acylethanolamide/endocannabinoid signaling system associated to memory impairments in postweaned rats. Front Neuroanat. 2015; 9:141
NO Journal Article;
DS RISalud
RD Apr 18, 2025