Palmitoylethanolamide Attenuates Perinatal Asphyxia-induced Damage in the Developing Rat Striatum

UDOVIN, LUCAS D., KOBIEC TAMARA; HERRERA, MARÍA I.; KUSNIER, CARLOS F.; AGUILAR, ANDREA P.; LUACES, JUAN P.; OTERO-LOSADA, MATILDE; CAPANI, FRANCISCO

MICROSCOPY & MICROANALYSIS

CAMBRIDGE UNIV PRESS

Año: 2020 vol. 26 p. 135 - 136

1431-9276

Lucas D. Udovin1 * Δ, Tamara Kobiec1 2 Δ, María I. Herrera1 2, Carlos F. Kusnier1, Andrea P. Aguilar1, JuanP. Luaces1, Matilde Otero-Losada1and Francisco Capani1 31. Instituto de Investigaciones Cardiológicas (ININCA), UBA-CONICET, CABA, Buenos Aires,Argentina.2. Centro de Investigaciones en Psicología y Psicopedagogía, Facultad de Psicología, Universidad CatólicaArgentina, Buenos Aires, Argentina.3. Departamento de Biología Facultad de Farmacia y Bioquímica, UAJFK.*. Corresponding author: lucas2304@hotmail.comΔ These authors contributed equally to this work.Perinatal asphyxia (PA) is the clinical condition brought by a birth temporary oxygen deprivationassociated with long-term damage in the corpus striatum. This is one of the most compromised brainaffected areas. Palmitoylethanolamide (PEA) is a neuromodulator well-known for its protective effects inbrain injury models including PA, albeit not deeply studied regarding its particular effects in the corpusstriatum following PA.Using the Bjelke et al. (1991) PA model [1], full-term pregnant rats were decapitated, and uterus hornsplaced in a water bath at 37°C for 19 min. One hour later, the pups were injected with PEA 10 mg /kg s.c.and placed with surrogate mothers. After 30 days, the animals were perfused, and coronal and striatalsections were collected to analyze protein level expression by western blot and the reactive area byimmunohistochemistry for neuron markers: Phosphorylated Neurofilament-Heavy/Medium chain (pNFH/M) and Microtubule-Associated Protein-2 (MAP-2) and the astrocyte marker, Glial fibrillary acidicprotein (GFAP).Results indicated that PA produced neuronal damage and morphological changes. Asphyctic rats showeda decrease in pNF-H/M and MAP-2 reactive areas, GFAP+ number cells, and MAP-2 and pNF-H/Mprotein expression in the striatum. Treatment with PEA partially restored the number of GFAP+ cells, andpartially prevented the decrease in pNF-H/M and MAP-2 reactive areas in asphyctic rats. Treatment withPEA also reversed the decrease in MAP-2 protein expression and partially prevented the decrease in pNFH/M protein expression in asphyctic rats. Perinatal asphyxia did not affect GFAP protein level.Treatment with PEA reduced striatal damage induced by PA, suggesting its therapeutic potential for theprevention of neurodevelopmental disorders.