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

Abstract

Early exposure to EtOH (EEE) triggers a spectrum of neurobehavioral dysfunctions, affecting the hypoxic ventilatory response-HVR, reducing Omega-3 (ω3) le els in the CNS, and increasing neuronal degeneration. This study analyzed the effects of EtOH and the protecti e action of ω3 on the HVR and some nuclei in ol ed 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 recei ed 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 N S. Besides, in the N S, ω3 showed a protecti e effect in IHE groups by decreasing the number of DN, corroborated by C3+ labeling. No protecti e effect of ω3 was obser ed in EtOH-exposed groups. In sum, EEE negatively affected HVR. At brainstem nuclei analyzed, an increase in the neuronal degeneration was obser ed as a function of both ethanol EEE and IHE. ω3 pro ided protection onl in the NTS and it reversed IHE-induced neurodegeneration.