ArticleMolecular neurobiology2014
Activation of liver X receptor is protective against ethanol-induced developmental impairment of Bergmann glia and Purkinje neurons in the mouse cerebellum.
Article in Molecular neurobiology, 2014. 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, 26 citations in OpenAlex.
- Developmental ethanol exposure has minimal impact on cerebellar microglial dynamics, morphology, and interactions with Purkinje cells during adolescence.Frontiers in neuroscience · 2023Article
- Loss of liver X receptor β in astrocytes leads to anxiety-like behaviors via regulating synaptic transmission in the medial prefrontal cortex in mice.Molecular psychiatry · 2021Article
- Caffeine consumption attenuates ethanol-induced inflammation through the regulation of adenosinergic receptors in the UChB rats cerebellum.Toxicology research · 2021Article
- Inhibitors of cellular stress overcome acute effects of ethanol on hippocampal plasticity and learning.Neurobiology of disease · 2020Article
- Targeting CYP2J2 to Enhance the Anti-Glioma Efficacy of Cannabinoid Receptor 2 Stimulation by Inhibiting the Pro-Angiogenesis Function of M2 Microglia.Frontiers in oncology · 2020Article
- Abnormal Cerebellar Development Is Involved in Dystonia-Like Behaviors and Motor Dysfunction of Autistic BTBR Mice.Frontiers in cell and developmental biology · 2020Article
- Stably maintained microtubules protect dopamine neurons and alleviate depression-like behavior after intracerebral hemorrhage.Scientific reports · 2018Article
- Liver X receptor β regulates the development of the dentate gyrus and autistic-like behavior in the mouse.Proceedings of the National Academy of Sciences of the United States of America · 2018Article
- Epothilone B Benefits Nigrostriatal Pathway Recovery by Promoting Microtubule Stabilization After Intracerebral Hemorrhage.Journal of the American Heart Association · 2018Article
- Activation of liver X receptor delayed the retinal degeneration of rd1 mice through modulation of the immunological function of glia.Oncotarget · 2017Article
- Propofol Exposure in Early Life Induced Developmental Impairments in the Mouse Cerebellum.Frontiers in cellular neuroscience · 2017Article
- LXR Regulation of Brain Cholesterol: From Development to Disease.Trends in endocrinology and metabolism: TEM · 2016Review
- Choline Ameliorates Deficits in Balance Caused by Acute Neonatal Ethanol Exposure.Cerebellum (London, England) · 2015Article
- Radial glia, the keystone of the development of the hippocampal dentate gyrus.Molecular neurobiology · 2015Review
- Liver X receptor β is essential for the differentiation of radial glial cells to oligodendrocytes in the dorsal cortex.Molecular psychiatry · 2014Article
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Authors and funding
10 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cerebellar Purkinje cell and granule cell development are coordinated by Bergmann glia, and are particularly sensitive to ethanol (EtOH) exposure. The liver X receptor (LXR) plays important roles in Bergmann glial development. However, the effect of LXR activation on EtOH-mediated impairment of Bergmann glia and subsequently on Purkinje cell dendritogenesis remains undetermined. Therefore, using immunohistochemistry, quantitative real-time PCR and Western blot, we tested the possible protection of LXR agonist T0901317 (T0) on Bergmann glia and Purkinje cell dendritogenesis in mice exposed to ethanol. Results showed that a brief exposure of EtOH on postnatal day (PD 5) significantly decreased the average body weight of mice at PD 6 without alteration in the brain weight. In EtOH-exposed mice, the number of migrating granule cells in the molecular layer was significantly decreased, and this effect was attenuated by pretreatment of T0. EtOH exposure also resulted in the significant reduction of calbindin-labeled Purkinje cells, their maximum dendrite length, and impairment of Purkinje cell dendritogenesis. Furthermore, EtOH induced the activation of microglia in the Purkinje cell layer and impaired the development of Bergmann glia. However, pretreatment of T0 effectively blocked all of these responses. These responses were found to be mediated by the inhibition of upregulated levels of β-catenin and transcription factor LEF1 in the cerebellum. Overall, the results suggest that activating LXRs on postnatal mice exposed to EtOH is protective to Bergmann glia, and thus may play a critical role in preventing EtOH-induced defects during cerebellar development.
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