Omega-3 but not Omega 6 mitigates Behavioral Impairments Induced by Binge Ethanol Exposure in Rat Neonates

Abstract

Maternal alcohol consumption during pregnancy may cause neurocognitive and behavioral disorders that canpersist until adulthood. Epidemiological data has revealed an alarming increase in the frequency of alcoholintake in pregnant women. Nutritional variables may also have an impact on the behavioral alterations occasioned by alcohol during development. Moreover, omega-3, a polyunsaturated fatty acid necessary fornormal brain development, is deficient in ethanol-treated animals. Although studies have shown that omega-3supplementation after prenatal ethanol (EtOH) treatment improves some disorders, there are no reports aboutacute treatment with omega-3 in binge alcohol neurotoxic models during postnatal development. The goalof this study was to determine whether an administration of omega-3, after an acute ethanol dose in neonates, would be able to attenuate alcohol effects in offspring. Male/ female rats were administered ethanol(2.5 g/kg s.c. at 0 and 2 h) or saline on postnatal day (PND) 7, with a single dose of omega-3 (720 mg/kg),or omega-6, 15 min after the last alcohol injection. It has been found that EtOH-treated animals showedhyperlocomotion and anxiety-like behavior on PND 14. Administration of omega-3 after EtOH treatmentreduced hyperlocomotion and the anxiety-like behaviors on PND 14. On the other hand, animals treated withomega-6 did not reduce those EtOH effects. In conclusion, acute ethanol exposure induced neurobehavioral alterations that persisted in the offspring and omega 3 mitigates those effects but not omega 6. These dataare relevant considering that omega-3 treatment may have therapeutic effects through mitigating some ofethanol´s damaging consequences.