Folate administration ameliorates neurobehavioral effects of prenatal ethanol exposure.
The American journal of drug and alcohol abuse(2023)
Abstract
Prenatal ethanol exposure (PEE) induces heightened ethanol intake at adolescence in preclinical studies. Ethanol intake alters the absorption of folate, a methyl-group donor critical for numerous cellular functions. The prenatal administration of folate is, therefore, a promising approach to reduce the effects of PEE. Experiment 1 determined if prenatal folate modulated the effects of PEE on ethanol intake, anxiety-like response, and exploratory behaviors (Experiment 1) in Wistar rats. Experiment 2 assessed, in rats not given PEE, if postnatal folate reversed effects of ethanol exposure at postnatal days 28-42. Experiment 3 assessed if folate altered blood ethanol levels (BELs). Experiment 1 involved 242 (125 male) adolescent Wistar rats derived from dams given folate (20 mg/kg, gestational days - GD- 13-20) + ethanol (2.0 g/kg, GD 17-20), ethanol, or vehicle only at pregnancy. Experiment 2 involved 29 male adolescents administered vehicle or ethanol doses co-administered or not with folate. In Experiment 3 twelve adult females were tested for BELs after folate administration. These tests were applied: intake tests, light dark box (LDB), elevated plus maze, open field and concentric square field. PEE heightened ethanol intake (η ps = 0.06-07) and induced hyperactivity and a reduced latency to exit the white area of the LDB (η ps = 0.12-17). These effects were partially inhibited by folate (p > .05). Rats exposed to ethanol exposure at adolescence exhibited reduced motor activity (η p = .17), regardless of folate treatment. Folate did not affect BELs. Folate administration should be considered as a preventive or acute treatment to attenuate the neurobehavioral effects of PEE.
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Key words
Prenatal ethanol exposure,adolescent rats,anxiety,folate,intermittent ethanol
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