info:eu-repo/semantics/article
Partial Reversal of Striatal Damage by Palmitoylethanolamide Administration Following Perinatal Asphyxia
Fecha
2020-01Registro en:
Udovin, Lucas; Kobiec, Tamara; Herrera, María Inés; Toro Urrego, Nicolas; Kusnier, Carlos Federico; et al.; Partial Reversal of Striatal Damage by Palmitoylethanolamide Administration Following Perinatal Asphyxia; Frontiers Media S.A.; Frontiers in Neuroscience; 13; 1-2020; 1-10
1662-4548
1662-453X
CONICET Digital
CONICET
Autor
Udovin, Lucas
Kobiec, Tamara
Herrera, María Inés
Toro Urrego, Nicolas
Kusnier, Carlos Federico
Kolliker Frers, Rodolfo Alberto
Ramos Hryb, Ana Belen
Luaces, Juan Pablo
Otero-losada, Matilde Estela
Capani, Francisco
Resumen
Perinatal asphyxia (PA) is a clinical condition brought by a birth temporary oxygen deprivation associated with long-term damage in the corpus striatum, one of the most compromised brain areas. Palmitoylethanolamide (PEA) is a neuromodulator well known for its protective effects in brain injury models, including PA, albeit not deeply studied regarding its particular effects in the corpus striatum following PA. Using Bjelke et al. (1991) PA model, full-term pregnant rats were decapitated, and uterus horns were placed 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 striatal sections were collected to analyze protein-level expression by Western blot and the reactive area by immunohistochemistry for neuron markers: phosphorylated neurofilament-heavy/medium-chain (pNF-H/M) and microtubule-associated protein-2 (MAP-2), and the astrocyte marker, glial fibrillary acidic protein (GFAP). Results indicated that PA produced neuronal damage and morphological changes. Asphyctic rats showed a decrease in pNF-H/M and MAP-2 reactive areas, GFAP+ cells number, and MAP-2 as well as pNF-H/M protein expression in the striatum. Treatment with PEA largely restored the number of GFAP+ cells. Most important, it ameliorated the decrease in pNF-H/M and MAP-2 reactive areas in asphyctic rats. Noticeably, PEA treatment reversed the decrease in MAP-2 protein expression and largely prevented PA-induced decrease in pNF-H/M protein expression. PA did not affect the GFAP protein level. Treatment with PEA attenuated striatal damage induced by PA, suggesting its therapeutic potential for the prevention of neurodevelopmental disorders.