ArticleBrain structure & function2019
Effects of neonatal ethanol on cerebral cortex development through adolescence.
Article in Brain structure & function, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 19 citations in OpenAlex.
- Four-year follow-up of a randomized controlled trial of choline for neurodevelopment in fetal alcohol spectrum disorder.Journal of neurodevelopmental disorders · 2020Trial
- Effects of ethanol exposure in neonatal mice on retinoic acid signaling in forebrain neurons and astrocytes.IBRO neuroscience reports · 2026Article
- No indication of histological changes in embryonic somatosensory cortex development upon maternal aspartame consumption in mice.NPJ science of food · 2026Article
- Defects of Cortical Microcircuits Following Early Exposure to Alcohol.Advances in experimental medicine and biology · 2025Review
- Developmental alcohol exposure is exhausting: Sleep and the enduring consequences of alcohol exposure during development.Neuroscience and biobehavioral reviews · 2024Review
- Early-life maturation of the somatosensory cortex: sensory experience and beyond.Frontiers in neural circuits · 2024Review
- Delayed cortical thinning in children and adolescents with prenatal alcohol exposure.Alcohol, clinical & experimental research · 2023Article
- Effects of retinoic acid receptor α modulators on developmental ethanol-induced neurodegeneration and neuroinflammation.Frontiers in neuroscience · 2023Article
- Somatostatin neuron contributions to cortical slow wave dysfunction in adult mice exposed to developmental ethanol.Frontiers in neuroscience · 2023Article
- Estimates of total neuron number show that neonatal ethanol causes immediate and lasting neuron loss in cortical and subcortical areas.Frontiers in neuroscience · 2023Article
- Homeostatic NREM sleep and salience network function in adult mice exposed to ethanol during development.Frontiers in neuroscience · 2023Article
- Neonatal ethanol causes profound reduction of cholinergic cell number in the basal forebrain of adult animals.Alcohol (Fayetteville, N.Y.) · 2021Article
- Perinatal interference with the serotonergic system affects VTA function in the adult via glutamate co-transmission.Molecular psychiatry · 2021Article
- Enhancement of parvalbumin interneuron-mediated neurotransmission in the retrosplenial cortex of adolescent mice following third trimester-equivalent ethanol exposure.Scientific reports · 2021Article
- Post-exposure environment modulates long-term developmental ethanol effects on behavior, neuroanatomy, and cortical oscillations.Brain research · 2020Article
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Authors and funding
8 authors at 2 institutions in 1 country.
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Abstract
Neonatal brain lesions cause deficits in structure and function of the cerebral cortex that sometimes are not fully expressed until adolescence. To better understand the onset and persistence of changes caused by postnatal day 7 (P7) ethanol treatment, we examined neocortical cell numbers, volume, surface area and thickness from neonatal to post-adolescent ages. In control mice, total neuron number decreased from P8 to reach approximately stable levels at about P30, as expected from normal programmed cell death. Cortical thickness reached adult levels by P14, but cortical volume and surface area continued to increase from juvenile (P20-30) to post-adolescent (P54-93) ages. P7 ethanol caused a reduction of total neurons by P14, but this deficit was transient, with later ages having only small and non-significant reductions. Previous studies also reported transient neuron loss after neonatal lesions that might be partially explained by an acute acceleration of normally occurring programmed cell death. GABAergic neurons expressing parvalbumin, calretinin, or somatostatin were reduced by P14, but unlike total neurons the reductions persisted or increased in later ages. Cortical volume, surface area and thickness were also reduced by P7 ethanol. Cortical volume showed evidence of a transient reduction at P14, and then was reduced again in post-adolescent ages. The results show a developmental sequence of neonatal ethanol effects. By juvenile ages the cortex overcomes the P14 deficit of total neurons, whereas P14 GABA cell deficits persist. Cortical volume reductions were present at P14, and again in post-adolescent ages.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.