Growth and behavioral differences in a C57BL/6J mouse model of prenatal alcohol exposure.

Autor: Mooney SM; Nutrition Research Institute, University of North Carolina at Chapel Hill, Kannapolis, NC 28081, USA; Department of Nutrition, University of North Carolina at Chapel Hill, Kannapolis, NC, 28081, USA., Pjetri E; Nutrition Research Institute, University of North Carolina at Chapel Hill, Kannapolis, NC 28081, USA., Friday WB; Nutrition Research Institute, University of North Carolina at Chapel Hill, Kannapolis, NC 28081, USA., Smith SM; Nutrition Research Institute, University of North Carolina at Chapel Hill, Kannapolis, NC 28081, USA; Department of Nutrition, University of North Carolina at Chapel Hill, Kannapolis, NC, 28081, USA. Electronic address: Susan_Smith@unc.edu.
Jazyk: angličtina
Zdroj: Alcohol (Fayetteville, N.Y.) [Alcohol] 2021 Dec; Vol. 97, pp. 51-57. Date of Electronic Publication: 2021 Sep 28.
DOI: 10.1016/j.alcohol.2021.09.031
Abstrakt: Background: Prenatal alcohol exposure (PAE) can produce behavioral deficits in the presence or absence of growth and morphological deficits. Here, we describe a murine PAE model having parallels to the clinical diagnosis of alcohol-related neurodevelopmental deficit (ARND).
Methods: Pregnant C57BL/6J mice were gavaged with alcohol (ALC, 3 g/kg) or maltodextrin daily on embryonic days (E) E8.5 through E17.5. Blood alcohol levels were 211 ± 14 mg/dL at 30 min post-gavage. Offspring behavior was tested at adolescence.
Results: ALC dams gained less weight during the alcohol exposure period (p = 0.035). ALC male and female pups weighed more than controls at P15 (p ≤ 0.001) and P22 (p ≤ 0.001), but not at P37, perhaps because their dams were pair-housed. During the training session for accelerating rotarod, control offspring trended to stay longer on the rotarod than did ALC offspring [F (1,54)  = 2.892, p = 0.095]. In the Y-maze, ALC offspring had a higher percent alternation than did controls [F (1,54)  = 16.577, p < 0.001], but activity level did not appear to differ. In the fear-conditioning test, there was no ALC effect in the training trial. In the contextual test, there was a group × minute effect for males [F (4,120)  = 2.94, p = 0.023], and ALC trended to freeze less than controls in minute 1 (p = 0.076) and froze less in minute 2 (p = 0.02). In the cue test, there was a trend for a group-sex interaction [F (1,53)  = 3.008, p = 0.089] on overall freezing, such that ALC males (p < 0.05) again froze less than control males, whereas ALC females (p < 0.05) froze more than control females.
Conclusions: This mouse model of PAE, using a repeated intermediate exposure, produces modest behavioral impairments that are consistent along the continuum of PAE models, including deficits in associative memory and hyper-responsivity. The lack of growth or morphological deficits suggests these mice may model aspects of ARND.
(Copyright © 2021 Elsevier Inc. All rights reserved.)
Databáze: MEDLINE
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