ArticleAmerican journal of obstetrics and gynecology2009
Prenatal NAP+SAL prevents developmental delay in a mouse model of Down syndrome through effects on N-methyl-D-aspartic acid and gamma-aminobutyric acid receptors.
Article in American journal of obstetrics and gynecology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers, 1 of them a synthesis that pooled it.
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Who cites it
12 citing papers in PubMed, 1 synthesis or guideline pooled it, 21 citations in OpenAlex.
- Prenatal and Postnatal Therapies for Down's Syndrome and Associated Developmental Anomalies and Degenerative Deficits: A Systematic Review of Guidelines and Trials.Frontiers in medicine · 2022Pooled it
- Quantitative Analysis of Retinal Structure and Function in Two Chromosomally Altered Mouse Models of Down Syndrome.Investigative ophthalmology & visual science · 2020Article
- Timing of therapies for Down syndrome: the sooner, the better.Frontiers in behavioral neuroscience · 2015Review
- Review
- Weaker control of the electrical properties of cerebellar granule cells by tonically active GABAA receptors in the Ts65Dn mouse model of Down's syndrome.Molecular brain · 2013Article
- Reducing GABAA α5 receptor-mediated inhibition rescues functional and neuromorphological deficits in a mouse model of down syndrome.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2013Article
- Article
- Mouse models of Down syndrome as a tool to unravel the causes of mental disabilities.Neural plasticity · 2012Review
- Effects of ethanol and NAP on cerebellar expression of the neural cell adhesion molecule L1.PloS one · 2011Article
- On the promise of pharmacotherapies targeted at cognitive and neurodegenerative components of Down syndrome.Developmental neuroscience · 2011Review
- Molecular basis of pharmacotherapies for cognition in Down syndrome.Trends in pharmacological sciences · 2010Review
- Behavioral validation of the Ts65Dn mouse model for Down syndrome of a genetic background free of the retinal degeneration mutation Pde6b(rd1).Behavioural brain research · 2010Article
Corrections and comments
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Authors and funding
6 authors at 4 institutions in 1 country.
Funding
Abstract
objectiveDown 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 gamma-aminobutyric acid (GABA) receptor subunits. STUDY
designPregnant 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 GABA(A)alpha5 and GABA(A)beta3 with glyceraldehyde-3-phosphate dehydrogenase standardization. Statistics included analysis of variance and Fisher PLSD with P < .05 as significant.
resultsNR2A, NR2B, and GABA(A)beta3 levels were decreased in Ts vs control (all P < .05). Prenatal NAP+SAL increased NR2A, NR2B, and GABA(A)beta3 to levels similar to control (all P < .05). A significant difference in GABA(A)alpha5 levels was not found.
conclusionPrenatal NAP+SAL increases NR2A, NR2B, and GABA(A)beta3 expression in adult DS mice to levels similar to controls. This may explain how NAP+SAL improve developmental milestone achievement.
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