ArticleCerebellum (London, England)2010
Altered cerebellar development in nuclear receptor TAK1/ TR4 null mice is associated with deficits in GLAST(+) glia, alterations in social behavior, motor learning, startle reactivity, and microglia.
Article in Cerebellum (London, England), 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 28 citations in OpenAlex.
- Deletion ofProceedings of the National Academy of Sciences of the United States of America · 2022Article
- DNA methylation changes in glial cells of the normal-appearing white matter in Multiple Sclerosis patients.Epigenetics · 2022Article
- Conditional knockout of UBC13 produces disturbances in gait and spontaneous locomotion and exploration in mice.Scientific reports · 2019Article
- Dopamine DBiological psychiatry · 2018Article
- Exploring the Wnt signaling pathway in schizophrenia and bipolar disorder.Translational psychiatry · 2018Article
- Article
- Di-(2-ethylhexyl) phthalate induces apoptosis of GC-2spd cells via TR4/Bcl-2 pathway.Environmental toxicology and pharmacology · 2016Article
- Alkaline Ceramidase 3 Deficiency Results in Purkinje Cell Degeneration and Cerebellar Ataxia Due to Dyshomeostasis of Sphingolipids in the Brain.PLoS genetics · 2015Article
- Inhibition-Based Biomarkers for Autism Spectrum Disorder.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2015Review
- Fast cerebellar reflex circuitry requires synaptic vesicle priming by munc13-3.Cerebellum (London, England) · 2015Article
- Lack of parvalbumin in mice leads to behavioral deficits relevant to all human autism core symptoms and related neural morphofunctional abnormalities.Translational psychiatry · 2015Article
- Role of Nuclear Receptors in Central Nervous System Development and Associated Diseases.Journal of experimental neuroscience · 2015Review
- Developmental treatment with ethinyl estradiol, but not bisphenol A, causes alterations in sexually dimorphic behaviors in male and female Sprague Dawley rats.Toxicological sciences : an official journal of the Society of Toxicology · 2014Article
- Minireview: Pathophysiological roles of the TR4 nuclear receptor: lessons learned from mice lacking TR4.Molecular endocrinology (Baltimore, Md.) · 2014Article
- Bergmann glia function in granule cell migration during cerebellum development.Molecular neurobiology · 2013Review
- Ablation of neuronal ceramide synthase 1 in mice decreases ganglioside levels and expression of myelin-associated glycoprotein in oligodendrocytes.The Journal of biological chemistry · 2012Article
- Genetic models of sensorimotor gating: relevance to neuropsychiatric disorders.Current topics in behavioral neurosciences · 2012Review
- Long-term Effects of Multiple Glucocorticoid Exposures in Neonatal Mice.Behavioral sciences (Basel, Switzerland) · 2011Article
- The clinical implications of mouse models of enhanced anxiety.Future neurology · 2011Article
- Increased acetylation in the DNA-binding domain of TR4 nuclear receptor by the coregulator ARA55 leads to suppression of TR4 transactivation.The Journal of biological chemistry · 2011Article
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Authors and funding
8 authors at 2 institutions in 1 country.
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Abstract
Previously, deficiency in the expression of the nuclear orphan receptor TAK1 was found to be associated with delayed cerebellar granule cell migration and Purkinje cell maturation with a permanent deficit in foliation of lobules VI–VII, suggesting a role for TAK1 in cerebellum development. In this study, we confirm that TAK1-deficient (TAK1(−/−)) mice have a smaller cerebellum and exhibit a disruption of lobules VI–VII. We extended these studies and show that at postnatal day 7, TAK1(−/−) mice exhibit a delay in monolayer maturation of dysmorphic calbindin 28K-positive Purkinje cells. The astrocyte-specific glutamate transporter (GLAST) was expressed within Bergmann fibers and internal granule cell layer at significantly lower levels in the cerebellum of TAK1(−/−) mice. At PND21, Golgi-positive Purkinje cells in TAK1(−/−) mice displayed a smaller soma (18%) and shorter distance to first branch point (35%). Neuronal death was not observed in TAK1(−/−) mice at PND21; however, activated microglia were present in the cerebellum, suggestive of earlier cell death. These structural deficits in the cerebellum were not sufficient to alter motor strength, coordination, or activity levels; however, deficits in acoustic startle response, prepulse startle inhibition, and social interactions were observed. Reactions to a novel environment were inhibited in a light/dark chamber, open-field, and home-cage running wheel. TAK1(−/−) mice displayed a plateau in performance on the running wheel, suggesting a deficit in learning to coordinate performance on a motor task. These data indicate that TAK1 is an important transcriptional modulator of cerebellar development and neurodevelopmentally regulated behavior.
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