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. 2013 Jun 25;8(18):1702-13.
doi: 10.3969/j.issn.1673-5374.2013.18.008.

A new treatment for cognitive disorders related to in utero exposure to alcohol

Shuang Li  1 , Yan Zhang  1 , Feng Zhu  2 , Bin Zhang  2 , Jianying Lin  2 , Chunyang Xu  3 , Wancai Yang  4 , Wei Hao  5 , Ruiling Zhang  5
Affiliations

A new treatment for cognitive disorders related to in utero exposure to alcohol

Shuang Li et al. Neural Regen Res. .

Abstract

Maternal alcohol consumption during pregnancy has detrimental effects on fetal central nervous system development. Maternal alcohol consumption prior to and during pregnancy significantly affects cognitive functions in offspring, which may be related to changes in cyclin-dependent kinase 5 because it is associated with modulation of synaptic plasticity and impaired learning and memory. In this study, we examined adult offspring in a maternal alcohol consumption model in rats. Y-maze test results showed that in utero exposure to alcohol impairs learning and memory capacities. Cyclin-dependent kinase 5 mRNA and protein expressions in the hippocampus of the offspring were significantly elevated, as assayed by quantitative real-time PCR and reverse transcription-PCR, immunofluorescence, and immuno-precipitation. Our experimental findings strongly suggest that altered cyclin-dependent kinase 5 may mediate impaired learning and memory in adult rats that were exposed to alcohol by maternal consumption while in utero.

Keywords: cyclin-dependent kinase 5; development; ethanol; grants-supported paper; hippocampus; learning and memory; neural regeneration; neurogenesis; neuroregeneration; offspring; pregnancy.

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Conflict of interest statement

Conflicts of interest: None declared.

Figures

Figure 1
Figure 1
Effects of maternal alcohol consumption on mRNA expression of cyclin-dependent kinase 5 (Cdk5) and p35 in the hippocampus of offspring (quantitative reverse transcription-PCR). Total RNA isolated and dissociated from the hippocampus of rats was reverse transcribed to produce PCR products then visualized on agarose gels. (A) Bands of p35 mRNA; (B) bands of Cdk5 mRNA. CN: Control group; IC: isocaloric group; ET: ethanol-treated group; M: marker.
Figure 2
Figure 2
Effects of maternal alcohol consumption on cyclin-dependent kinase 5 (Cdk5) and p35 expression in the hippocampus of rat offspring (immunofluorescence, × 400). (A, B) Bar graph of Cdk5- and p35-positive cell numbers in the hippocampus. aP < 0.01, vs. CN and IC. Data are expressed as mean ± SD,n= 18 rats in each group. The experiment was repeated three times, and analyzed using one-way analysis of variance and the least significant difference multiple-range test. (C) Representative photomicrographs of Cdk5 (Alexa Fluor 488-labeled, green fluorescence) and p35 (Cy3-labeled, red fluorescence) with immunofluorescent staining in the rat hippocampus. Scale bars: 10 μm. Cells with Cdk5 expression are green (white arrows). In contrast, cells with p35 expression are red (yellow arrows). Compared with the control and isocaloric groups, a large number of hippocampal neurons were stained with fluorescence in the offspring from the ethanol-treated group, and the density and fluorescence intensity increased. CN: Control group; ET: ethanol-treated group; IC: isocaloric group.
Figure 3
Figure 3
Effects of maternal alcohol consumption during pregnancy on cyclin-dependent kinase 5 (Cdk5) activity in the hippocampus of rat offspring. aP < 0.01, vs. control group. Cdk5 activity is expressed as p moles of ATP incorporated/mg protein per minute and is plotted as mean ± SD,n = 18 rats in each group. The experiment was repeated three times over five independent experiments. One-way analysis of variance and the least significant difference multiple-range test were used to determine differences between means. CN: Control group; ET: ethanol-treated group; IC: isocaloric group.
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