ReviewCerebellum (London, England)2004
The effects of ethanol on the developing cerebellum and eyeblink classical conditioning.
Review in Cerebellum (London, England), 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers, 1 of them a synthesis that pooled it.
What it found
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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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
34 citing papers in PubMed, 1 synthesis or guideline pooled it, 62 citations in OpenAlex.
- Recent breakthroughs in understanding the cerebellum's role in fetal alcohol spectrum disorder: A systematic review.Alcohol (Fayetteville, N.Y.) · 2024Pooled it
- Animal Models of Prenatal Alcohol Exposure.Advances in experimental medicine and biology · 2026Review
- High-resolution imaging in studies of alcohol effect on prenatal development.Advances in drug and alcohol research · 2023Article
- The effects of gestational choline supplementation on cerebellar Purkinje cell number in the sheep model of binge alcohol exposure during the first trimester-equivalent.Alcohol (Fayetteville, N.Y.) · 2022Article
- Mechanisms of Ethanol-Induced Cerebellar Ataxia: Underpinnings of Neuronal Death in the Cerebellum.International journal of environmental research and public health · 2021Review
- Characterization of motor function in mice developmentally exposed to ethanol using the Catwalk system: Comparison with the triple horizontal bar and rotarod tests.Behavioural brain research · 2021Article
- Video-based data acquisition system for use in eye blink classical conditioning procedures in sheep.Behavior research methods · 2017Article
- Ethanol exposure during development reduces GABAergic/glycinergic neuron numbers and lobule volumes in the mouse cerebellar vermis.Neuroscience letters · 2016Article
- Electrophysiological and Immunohistochemical Evidence for an Increase in GABAergic Inputs and HCN Channels in Purkinje Cells that Survive Developmental Ethanol Exposure.Cerebellum (London, England) · 2015Article
- White matter integrity of the cerebellar peduncles as a mediator of effects of prenatal alcohol exposure on eyeblink conditioning.Human brain mapping · 2015Article
- Eyeblink conditioning: a non-invasive biomarker for neurodevelopmental disorders.Journal of autism and developmental disorders · 2015Review
- Third trimester-equivalent ethanol exposure does not alter complex spikes and climbing fiber long-term depression in cerebellar Purkinje neurons from juvenile rats.Alcoholism, clinical and experimental research · 2014Article
- Repeated intermittent alcohol exposure during the third trimester-equivalent increases expression of the GABA(A) receptor δ subunit in cerebellar granule neurons and delays motor development in rats.Neuropharmacology · 2014Article
- Aging in the cerebellum and hippocampus and associated behaviors over the adult life span of CB6F1 mice.Neuroscience · 2013Article
- Neonatal ethanol exposure results in dose-dependent impairments in the acquisition and timing of the conditioned eyeblink response and altered cerebellar interpositus nucleus and hippocampal CA1 unit activity in adult rats.Alcohol (Fayetteville, N.Y.) · 2013Article
- Lysine acetyltransferases CBP and p300 as therapeutic targets in cognitive and neurodegenerative disorders.Current pharmaceutical design · 2013Review
- Long-term alterations of striatal parvalbumin interneurons in a rat model of early exposure to alcohol.Journal of neurodevelopmental disorders · 2012Article
- Choline supplementation mitigates trace, but not delay, eyeblink conditioning deficits in rats exposed to alcohol during development.Hippocampus · 2012Article
- Mechanisms of ethanol-induced death of cerebellar granule cells.Cerebellum (London, England) · 2012Review
- Magnetic resonance-based imaging in animal models of fetal alcohol spectrum disorder.Neuropsychology review · 2011Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
1 author at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
In rats, developmental ethanol exposure has been used to model the central nervous system deficits associated with human fetal alcohol syndrome. Binge-like ethanol exposure of neonatal rats depletes cells in the cerebellum, including Purkinje cells, granule cells, and deep nuclear cells, and produces deficits in simple tests of motor coordination. However, the extent to which anatomical damage is related to behavioral deficits has been difficult to estimate. Eyeblink classical conditioning is known to engage a discrete brain stem-cerebellar circuit, making it an ideal test of cerebellar functional integrity after developmental ethanol exposure. Eyeblink conditioning is a simple form of motor learning in which a neutral stimulus (such as a tone) comes to elicit an eyeblink when repeatedly paired with a stimulus that evokes an eyeblink prior to training (such as mild periorbital stimulation). In eyeblink conditioning, one of the deep cerebellar nuclei, the interpositus nucleus, as well as specific Purkinje cell populations, are sites of convergence for tone conditioned stimulus and somatosensory unconditioned stimulus information, and, together with brain stem nuclei, provide the necessary and sufficient substrate for the learned response. A series of studies have shown that eyeblink conditioning is impaired in both weanling and adult rats given binge-like exposure to ethanol as neonates. In addition, interpositus nucleus neurons from ethanol-exposed rats showed impaired activation during eyeblink conditioning. These deficits are accompanied by a permanent reduction In the deep cerebellar nuclear cell population. Because particular cerebellar cell populations are utilized in well-defined ways during eyeblink conditioning, conclusions regarding the underlying neural substrates of behavioral change after developmental ethanol exposure are greatly strengthened.
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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.