Abstract
Objective: Down syndrome (DS) affects 1/800 infants. Prenatal NAPVSIPQ (NAP) and SALLRSIPA (SAL) (NAP+SAL) prevent developmental delay in Ts65Dn mice, a mouse model of DS. We investigated whether this finding involves N-methyl-D-aspartic acid and γ-aminobutyric acid (GABA) receptor subunits. Study Design: Pregnant Ts65Dn mice were treated with placebo or NAP+SAL on gestational days 8-12. After developmental delay prevention was shown, 4 trisomic (Ts), 4 control, and 3 Ts+NAP+SAL adult offspring brains (from 3 litters) were collected. Calibrator-normalized real-time polymerase chain reaction was performed using primers for N-methyl-D-aspartic acid subunits NR2A and NR2B, and for GABA subunits GABAAα5 and GABAAβ3 with glyceraldehyde-3-phosphate dehydrogenase standardization. Statistics included analysis of variance and Fisher PLSD with P < .05 as significant. Results: NR2A, NR2B, and GABAAβ3 levels were decreased in Ts vs control (all P < .05). Prenatal NAP+SAL increased NR2A, NR2B, and GABAAβ3 to levels similar to control (all P < .05). A significant difference in GABAAα5 levels was not found. Conclusion: Prenatal NAP+SAL increases NR2A, NR2B, and GABAAβ3 expression in adult DS mice to levels similar to controls. This may explain how NAP+SAL improve developmental milestone achievement.
Original language | English (US) |
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Pages (from-to) | 524.e1-524.e4 |
Journal | American journal of obstetrics and gynecology |
Volume | 200 |
Issue number | 5 |
DOIs | |
State | Published - May 2009 |
Externally published | Yes |
Keywords
- Down syndrome
- N-methyl-D-aspartic acid
- NAPVSIPQ
- SALLRSIPA
- Ts65Dn
- learning
- γ-aminobutyric acid
ASJC Scopus subject areas
- Obstetrics and Gynecology