Reversal of alcohol-induced learning deficits in the young adult in a model of fetal alcohol syndrome
Obstetrics and Gynecology, ISSN: 0029-7844, Vol: 115, Issue: 2 PART 1, Page: 350-356
2010
- 30Citations
- 47Captures
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Metrics Details
- Citations30
- Citation Indexes30
- 30
- CrossRef19
- Captures47
- Readers47
- 47
Article Description
OBJECTIVE: To evaluate whether treatment with neuroprotective peptides to young adult mice prenatally exposed to alcohol reverses alcohol-induced learning deficits in a mouse model of fetal alcohol syndrome, whether the mechanism involves the N-methyl-d-aspartate (NMDA) and γ-aminobutyric acid type A (GABAA) receptors, and whether it is related to glial cells. METHODS: C57Bl6/J mice were treated with alcohol (0.03 ml/g) or placebo on gestational day 8. On day 40, male mice exposed to alcohol in utero were treated daily for 10 days with D-NAPVSIPQ and D-SALLRSIPA (n=20) or placebo (n=13); and control offspring were treated with placebo (n=46), with the treatment blinded. Learning evaluation began after 3 days using the Morris watermaze and the T-maze. The hippocampus, cortex, and cerebellum were isolated. Expression of NR2A, NR2B, GABAAβ3, GABAAα5, vasoactive intestinal peptide (VIP), activity-dependent neuroprotective protein, and glial fibrillary acidic protein was measured using calibrator-normalized relative real-time polymerase chain reaction. Statistical analysis included analysis of variance and Fisher's protected least significant difference. Results: Treatment with D-NAPVSIPQ and D-SALLRSIPA reversed the alcohol-induced learning deficit in both learning tests as well as the NR2A and NR2B down-regulation in the hippocampus and the up-regulation of NR2A in the cortex and NR2B in the cortex and cerebellum (all P<.05). No significant differences were found in GABAA expression. Moreover, the peptides changed activity-dependent neuroprotective protein expression in the cortex (P=.016) but not the down-regulation of VIP (P=.883), probably because the peptides are downstream from VIP. Conclusion: Alcohol-induced learning deficit was reversed and expression of NR2A and NR2B was restored in the hippocampus and cortex of young adult mice treated with D-NAPVSIPQ and D-SALLRSIPA. Given the role of NMDA receptors in learning, this may explain in part the mechanism of prevention of alcohol-induced learning deficits by D-NAPVSIPQ and D-SALLRSIPA. © 2010 by The American College of Obstetricians and Gynecologists. Published by Lippincott Williams & Wilkins.
Bibliographic Details
http://www.scopus.com/inward/record.url?partnerID=HzOxMe3b&scp=76549101309&origin=inward; http://dx.doi.org/10.1097/aog.0b013e3181cb59da; http://www.ncbi.nlm.nih.gov/pubmed/20093910; http://content.wkhealth.com/linkback/openurl?sid=WKPTLP:landingpage&an=00006250-201002000-00022; https://journals.lww.com/00006250-201002000-00022; https://dx.doi.org/10.1097/aog.0b013e3181cb59da; https://journals.lww.com/greenjournal/Fulltext/2010/02000/Reversal_of_Alcohol_Induced_Learning_Deficits_in.22.aspx
Ovid Technologies (Wolters Kluwer Health)
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