Abstract
We evaluated a 9-amino-acid peptide, SALLRSIPA (SAL), an agonist of activity-dependent neurotrophic factor (ADNF), for its protective properties against fetal alcohol-related brain growth retardation, using an established liquid diet model of alcohol-related neurodevelopmental disorder (ARND) in C57BL/6 mice. Alcohol exposure during neurulation reduced body weight, head size, and specifically brain weight and volume. Major gross brain deficits include underdevelopment of brain areas, cortical thinning, ventricle enlargement, and restricted midline neural tissue growth leading to openings at the roof/floor plate. SALLRSIPA (SAL) treatment increased fetal body weight and restored brain weight, brain volume, and regional brain size. Furthermore, SAL restored cortical thickness, reduced the size and frequency of neural tube openings, and attenuated ventricular enlargement. The ability of SAL to antagonize alcohol-retarded brain growth and development of forebrain and midline neural tube at midgestation suggests its potential use as an antagonist against fetal alcohol-rendered microencephaly early in development.
Original language | English (US) |
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Pages (from-to) | 189-199 |
Number of pages | 11 |
Journal | Journal of Molecular Neuroscience |
Volume | 24 |
Issue number | 2 |
DOIs | |
State | Published - Sep 2004 |
Externally published | Yes |
Keywords
- Brain development
- Fetal alcohol effect
- Fetal alcohol syndrome
- Microencephaly
- Neurotrophic factor
ASJC Scopus subject areas
- Cellular and Molecular Neuroscience