ArticleNeuroscience2012
Lithium prevents long-term neural and behavioral pathology induced by early alcohol exposure.
Article in Neuroscience, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
34 citing papers in PubMed, 47 citations in OpenAlex.
- Effects of ethanol exposure in neonatal mice on retinoic acid signaling in forebrain neurons and astrocytes.IBRO neuroscience reports · 2026Article
- Review
- Homeostatic NREM sleep and salience network function in adult mice exposed to ethanol during development.Frontiers in neuroscience · 2023Article
- Effects of retinoic acid receptor α modulators on developmental ethanol-induced neurodegeneration and neuroinflammation.Frontiers in neuroscience · 2023Article
- Ethanol sustains phosphorylated tau protein in the cultured neonatal rat hippocampus: Implications for fetal alcohol spectrum disorders.Alcohol (Fayetteville, N.Y.) · 2022Article
- Corticostriatal Circuit Models of Cognitive Impairments Induced by Fetal Exposure to Alcohol.Biological psychiatry · 2021Review
- Post-exposure environment modulates long-term developmental ethanol effects on behavior, neuroanatomy, and cortical oscillations.Brain research · 2020Article
- Postnatal Ethanol-Induced Neurodegeneration Involves CB1R-Mediated β-Catenin Degradation in Neonatal Mice.Brain sciences · 2020Article
- Neonatal Ethanol Disturbs the Normal Maturation of Parvalbumin Interneurons Surrounded by Subsets of Perineuronal Nets in the Cerebral Cortex: Partial Reversal by Lithium.Cerebral cortex (New York, N.Y. : 1991) · 2019Article
- CB1R regulates CDK5 signaling and epigenetically controls Rac1 expression contributing to neurobehavioral abnormalities in mice postnatally exposed to ethanol.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2019Article
- Activity-dependent Signaling and Epigenetic Abnormalities in Mice Exposed to Postnatal Ethanol.Neuroscience · 2018Article
- Sevoflurane-induced memory impairment in the postnatal developing mouse brain.Experimental and therapeutic medicine · 2018Article
- Developmental Ethanol-Induced Sleep Fragmentation, Behavioral Hyperactivity, Cognitive Impairment and Parvalbumin Cell Loss are Prevented by Lithium Co-treatment.Neuroscience · 2018Article
- CB1R-Mediated Activation of Caspase-3 Causes Epigenetic and Neurobehavioral Abnormalities in Postnatal Ethanol-Exposed Mice.Frontiers in molecular neuroscience · 2018Article
- Long Term Depression in Rat Hippocampus and the Effect of Ethanol during Fetal Life.Brain sciences · 2017Review
- Ethanol-Induced Neurodegeneration and Glial Activation in the Developing Brain.Brain sciences · 2016Review
- Developmental ethanol exposure-induced sleep fragmentation predicts adult cognitive impairment.Neuroscience · 2016Article
- Lithium Protects Against Anaesthesia Neurotoxicity In The Infant Primate Brain.Scientific reports · 2016Article
- Fetal Alcohol Spectrum Disorder: Potential Role of Endocannabinoids Signaling.Brain sciences · 2015Review
- Article
Corrections and comments
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Authors and funding
5 authors at 3 institutions in 2 countries.
Funding
Abstract
Fetal alcohol exposure can cause developmental defects in offspring known as fetal alcohol spectrum disorder (FASD). FASD symptoms range from obvious facial deformities to changes in neuroanatomy and neurophysiology that disrupt normal brain function and behavior. Ethanol exposure at postnatal day 7 in C57BL/6 mice induces neuronal cell death and long-lasting neurobehavioral dysfunction. Previous work has demonstrated that early ethanol exposure impairs spatial memory task performance into adulthood and perturbs local and interregional brain circuit integrity in the olfacto-hippocampal pathway. Here we pursue these findings to examine whether lithium prevents anatomical, neurophysiological, and behavioral pathologies that result from early ethanol exposure. Lithium has neuroprotective properties that have been shown to prevent ethanol-induced apoptosis. Here we show that mice co-treated with lithium on the same day as ethanol exposure exhibit dramatically reduced acute neurodegeneration in the hippocampus and retain hippocampal-dependent spatial memory as adults. Lithium co-treatment also blocked ethanol-induced disruption in synaptic plasticity in slice recordings of hippocampal CA1 in the adult mouse brain. Moreover, long-lasting dysfunctions caused by ethanol in olfacto-hippocampal networks, including sensory-evoked oscillations and resting state coherence, were prevented in mice co-treated with lithium. Together, these results provide behavioral and physiological evidence that lithium is capable of preventing or reducing immediate and long-term deleterious consequences of early ethanol exposure on brain function.
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Registered trials
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.