Neurochemistry and Neuropharmacology
Author: Ricardo Marcos Pautassi | Email: rpautassi@gmail.com
Ricardo Marcos Pautassi 1°, Leonardo Marengo 1°, Agostina Barey 1°, Agustín Salguero 1°, María Carolina Fabio 1°, Cruz Miguel Cendán 2°, Ignacio Morón-Henche 3°, Claudio D’Addario 4°
1° Instituto Ferreyra (INIMEC-CONICET, Universidad Nacional de Córdoba), Argentina
2° Department of Pharmacology, Institute of Neuroscience, Biomedical Research Center (CIBM) Faculty of Medicine, University of Granada and Biosanitary Research Institute ibs. Granada, Granada, Spain.
3° Department of Psychobiology and Centre of Investigation of Mind, Brain, and Behaviour (CIMCYC), University of Granada, Granada, Spain
4° Università degli Studi di Teramo, Italy
Prenatal exposure to ethanol (PEE) results in various neurobehavioral deficits in the developing fetus. In rats, the period spanning postnatal days (PDs) 4-9 corresponds to the human third trimester of gestation and is characterized by rapid synaptogenesis, myelination, and maturation of crucial brain structures and transmitter systems. Seeking potential remedies to counteract the harmful impacts of PEE, researchers have turned their attention to nutritional supplements like folate, a member of the vitamin B family that plays a vital role in DNA synthesis, amino acid metabolism, and strengthening antioxidant defenses. We assessed anxiety responses, open field activity and ethanol intake in male and female rats that, on PDs 4-9, had been administered ethanol (0.0 or 5 g/kg/day) preceded by folate (0.0 or 20 mg/kg). Neonatal exposure to ethanol did not modify anxiety responses nor exploratory activity but led to reduced body weight during infancy and reduced ethanol intake at adolescence. The latter effect, which likely reflects conditioned aversion derived from the pairing of ethanols sensory and pharmacological effects, was countered by folate administration. Folate also ameliorated ethanol-induced reductions in body weight. These findings suggest that folate, a treatment with minimal adverse effects, holds the potential to modulate neurobehavioral consequences of prenatal ethanol exposure.