Neuroprotective effect of Palmitoylethanolamide in behavioral and hippocampal alterations induced by perinatal asphyxia.

LUCAS D. UDOVIN

Congreso; XI Congreso internacional de investigación y práctica profesional en psicología; 2019

Facultad de Psicología UBA

Perinatal asphyxia (PA) is caused by low oxygen availability during delivery, which has been associated with brain damage, being the hippocampus one of the most affected structures. Palmitoethanolamide (PEA) is an endocannabinoid with neuroprotective effects. Using the PA murine model of Bjelke et al. (1991), which reproduces the clinical conditions of child birth, we aimed to evaluate the action of PEA in the immature brain. For this purpose, neonatal rats were asphyxiated and immediately injected with PEA (10 mg/kg). One month after PA, behavior was studied throughout Open Field (OF) and Elevated Plus Maze (EPM) Tests. Rats were then perfused and sections of the hippocampus were collected for morphological analysis. PA and PEA effects were analyzed by immunohistochemistry and Western Blot for neuron markers (pNF H/M and MAP-2) and the glial marker GFAP. Results indicated that PA induced vertical exploration impairments, anxiety-related behaviors, an increase in pNF H/M and a decrease in MAP-2 reactive area. These changes were confirmed by Western Blot. GFAP did not show significant changes after PA. Treatment with PEA attenuated PA-induced cellular and molecular hippocampal damage and its corresponding behavioral alterations.