Prenatal NAP+SAL prevents developmental delay in a mouse model of Down syndrome through effects on N-methyl-D-aspartic acid and γ-aminobutyric acid receptors

Joy Vink, Maddelena Incerti, Laura Toso, Robin Roberson, Daniel Abebe, Catherine Y. Spong

Research output: Contribution to journalArticle

20 Scopus citations


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 languageEnglish (US)
Pages (from-to)524.e1-524.e4
JournalAmerican journal of obstetrics and gynecology
Issue number5
StatePublished - May 2009



  • Down syndrome
  • N-methyl-D-aspartic acid
  • Ts65Dn
  • learning
  • γ-aminobutyric acid

ASJC Scopus subject areas

  • Obstetrics and Gynecology

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