V-023 | Neuroprotection of Omega-3 against the deleterious effects induced by ethanol and hypoxia in neonate rats

Cellular and Molecular Neurobiology
Author: Marisol Magali Segovia | Email: marisol.segovia@unc.edu.ar

Marisol Magali Segovia^1°2°, Verónica Balaszczuk^1°2°,Ana Fabiola Macchione

^1° Instituto de Investigaciones Psicológicas IIPsi-CONICET-UNC. Córdoba-Argentina
^2° Facultad de Psicología, UNC. Córdoba-Argentina

Early exposure to EtOH (EEE) triggers a spectrum of neurobehavioral dysfunctions, affecting the hypoxic ventilatory response-HVR, reducing Omega-3 (ω3) levels in the CNS, and increasing neuronal degeneration. This study analyzed the effects of EtOH and the protective action of ω3 on the HVR and some nuclei involved in this response. Pups were administered 2.0 or 0.0 g/kg EtOH by i.g on postnatal days-PD 3-5-7-9. On PD 3-5-7, pups received 0.0 or 720 mg/kg of ω3 i.g., 20 min after the EtOH-administration. On PD9, pups were subjected to an intermittent hypoxia event-IHE for 35 min. Brainstem were collected to evaluate the number of dark neurons-DN and caspase-3 (C3) positive neurons. We found that EtOH induced respiratory depressions during the HVR and fewer apneas during recovery normoxia periods than water-treated pups. ω3 did not modify either ventilatory responses. Exposure to IHE significantly increased the number of DN in the raphe magnus and raphe obscurus and had a synergistic effect with EtOH, increasing the number of DN in the NTS. Besides, in the NTS, ω3 showed a protective effect in IHE groups by decreasing the number of DN, corroborated by C3+ labeling. No protective effect of ω3 was observed in EtOH-exposed groups. In sum, EEE negatively affected HVR. At brainstem nuclei analyzed, an increase in the neuronal degeneration was observed as a function of both ethanol EEE and IHE. ω3 provided protection only in the NTS and it reversed IHE-induced neurodegeneration.