ArticleAlcoholism, clinical and experimental research2008
Peptidergic agonists of activity-dependent neurotrophic factor protect against prenatal alcohol-induced neural tube defects and serotonin neuron loss.
Article in Alcoholism, clinical and experimental research, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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10 citing papers in PubMed, 27 citations in OpenAlex.
- Article
- Persistent behavioral effects following early life exposure to retinoic acid or valproic acid in zebrafish.Neurotoxicology · 2016Article
- The impact of micronutrient supplementation in alcohol-exposed pregnancies on information processing skills in Ukrainian infants.Alcohol (Fayetteville, N.Y.) · 2015Article
- Article
- The serotonergic anatomy of the developing human medulla oblongata: implications for pediatric disorders of homeostasis.Journal of chemical neuroanatomy · 2011Review
- From research to practice: an integrative framework for the development of interventions for children with fetal alcohol spectrum disorders.Neuropsychology review · 2011Review
- Focus on: the use of animal models for the study of fetal alcohol spectrum disorders.Alcohol research & health : the journal of the National Institute on Alcohol Abuse and Alcoholism · 2011Review
- Focus on: neurotransmitter systems.Alcohol research & health : the journal of the National Institute on Alcohol Abuse and Alcoholism · 2011Review
- Fetal alcohol spectrum disorders: experimental treatments and strategies for intervention.Alcohol research & health : the journal of the National Institute on Alcohol Abuse and Alcoholism · 2011Review
- A neurodevelopmental framework for the development of interventions for children with fetal alcohol spectrum disorders.Alcohol (Fayetteville, N.Y.)Review
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
introductionPrenatal alcohol exposure via maternal liquid diet consumption by C57BL/6 (B6) mice causes conspicuous midline neural tube deficit (dysraphia) and disruption of genesis and development of serotonin (5-HT) neurons in the raphe nuclei, together with brain growth retardation. The current study tested the hypothesis that concurrent treatment with either an activity-dependent neurotrophic factor (ADNF) agonist peptide [SALLRSIPA, (SAL)] or an activity-dependent neurotrophic protein (ADNP) agonist peptide [NAPVSIPQ, (NAP)] would protect against these alcohol-induced deficits in brain development.
methodsTimed-pregnant B6 dams consumed alcohol from embryonic day 7 (E7, before the onset of neurulation) until E15. Fetuses were obtained on E15 and brain sections processed for 5-HT immunocytochemistry, for evaluation of morphologic development of the brainstem raphe and its 5-HT neurons. Additional groups were treated either with SAL or NAP daily from E7 to E15 to assess the potential protective effects of these peptides. Measures of incomplete occlusion of the ventral canal and the frequency and extent of the openings in the rhombencephalon were obtained to assess fetal dysraphia. Counts of 5-HT-immunostained neurons were also obtained in the rostral and caudal raphe.
resultsPrenatal alcohol exposure resulted in abnormal openings along the midline and delayed closure of ventral canal in the brainstem. This dysraphia was associated with reductions in the number of 5-HT neurons both in the rostral raphe nuclei (that gives rise to ascending 5-HT projections) and in the caudal raphe (that gives rise to the descending 5-HT projections). Concurrent treatment of the alcohol-consuming dams with SAL prevented dysraphia and protected against the alcohol-induced reductions in 5-HT neurons in both the rostral and caudal raphe. NAP was less effective in protecting against dysraphia and did not protect against 5-HT loss in the rostral raphe, but did protect against loss in the caudal raphe.
conclusionsThese findings further support the potential usefulness of these peptides for therapeutic interventions in pregnancies at risk for alcohol-induced developmental deficits. Notably, the ascending 5-HT projections of the rostral raphe have profound effects in regulating forebrain development and function, and the descending 5-HT projections of the caudal raphe are critical for regulating respiration. Protection of the rostral 5-HT-system may help prevent structural and functional deficits linked to abnormal forebrain development, and protection of the caudal systems may also reduce the increased risk for sudden infant death syndrome associated with prenatal alcohol exposure.
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