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|Título :||Palmitoylethanolamide attenuates neurodevelopmental delay and early hippocampal damage following perinatal asphyxia in rats||Autor :||Herrera, María Inés
Udovin, Lucas D.
Toro Urrego, Nicolás
Kusnier, Carlos F.
Kölliker Frers, Rodolfo A.
Luaces, Juan P.
Otero Losada, Matilde
|Palabras clave :||ASFIXIA PERINATAL; NEUROPROTECCION; PALMITOILETANOLAMIDA; DAÑO CEREBRAL||Fecha de publicación :||2022||Editorial :||Frontiers Media||Cita :||Herrera, M. I. Palmitoylethanolamide attenuates neurodevelopmental delay and early hippocampal damage following perinatal asphyxia in rats [en línea]. Frontiers in behavioral neuroscience. 2022, 16, 953157. doi: https://doi.org/10.3389/fnbeh.2022.953157. Disponible en: https://repositorio.uca.edu.ar/handle/123456789/15243||Proyecto:||Neuroprotección en asfixia perinatal. Una aproximación traslacional||Resumen :||Impaired gas exchange close to labor causes perinatal asphyxia (PA), a neurodevelopmental impairment factor. Palmitoylethanolamide (PEA) proved neuroprotective in experimental brain injury and neurodegeneration models. This study aimed to evaluate PEA effects on the immature-brain, i.e., early neuroprotection by PEA in an experimental PA paradigm. Newborn rats were placed in a 37◦C water bath for 19 min to induce PA. PEA 10 mg/kg, s.c., was administered within the first hour of life. Neurobehavioral responses were assessed from postnatal day 1 (P1) to postnatal day 21 (P21), recording the day of appearance of several reflexes and neurological signs. Hippocampal CA1 area ultrastructure was examined using electron microscopy. Microtubuleassociated protein 2 (MAP-2), phosphorylated high and medium molecular weight neurofilaments (pNF H/M), and glial fibrillary acidic protein (GFAP) were assessed using immunohistochemistry and Western blot at P21. Over the first 3 weeks of life, PA rats showed late gait, negative geotaxis and eye-opening onset, and delayed appearance of air-righting, auditory startle, sensory eyelid, forelimb placing, and grasp reflexes. On P21, the hippocampal CA1 area showed signs of neuronal degeneration and MAP-2 deficit. PEA treatment reduced PA-induced hippocampal damage and normalized the time of appearance of gait, air-righting, placing, and grasp reflexes. The outcome of this study might prove useful in designing intervention strategies to reduce early neurodevelopmental delay following PA...||URI :||https://repositorio.uca.edu.ar/handle/123456789/15243||ISSN :||1662-5153 (online)||Disciplina:||PSICOLOGIA||DOI:||10.3389/fnbeh.2022.953157||Derechos:||Acceso abierto|
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