ArticleNeuroscience2006
11beta-Hydroxysteroid dehydrogenase type 2 protects the neonatal cerebellum from deleterious effects of glucocorticoids.
Article in Neuroscience, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.
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Who cites it
37 citing papers in PubMed, 87 citations in OpenAlex.
- Control of sodium appetite by hindbrain aldosterone-sensitive neurons.Molecular and cellular endocrinology · 2024Review
- Glucocorticoid effects on the brain: from adaptive developmental plasticity to allostatic overload.The Journal of experimental biology · 2024Review
- Neurodevelopment at 24 months corrected age in extremely preterm infants treated with dexamethasone alternatives during the late postnatal period: a cohort study.European journal of pediatrics · 2024Observational
- 11ß hydroxysteroid dehydrogenases regulate circulating glucocorticoids but not central gene expression.General and comparative endocrinology · 2021Article
- Premature Birth and Developmental Programming: Mechanisms of Resilience and Vulnerability.Frontiers in psychiatry · 2020Review
- Aldosterone-sensitive HSD2 neurons in mice.Brain structure & function · 2019Article
- Sonic Hedgehog Agonist Protects Against Complex Neonatal Cerebellar Injury.Cerebellum (London, England) · 2018Article
- Aberrant Development and Synaptic Transmission of Cerebellar Cortex in a VPA Induced Mouse Autism Model.Frontiers in cellular neuroscience · 2018Article
- 11β-HSD Types 1 and 2 in the Songbird Brain.Frontiers in endocrinology · 2018Article
- Changes in 11β-Hydroxysteroid Dehydrogenase and Glucocorticoid Receptor Expression in Kawasaki Disease.Korean circulation journal · 2017Article
- Pharmacological approaches to intervention in hypomyelinating and demyelinating white matter pathology.Neuropharmacology · 2016Review
- Conditional Deletion of Hsd11b2 in the Brain Causes Salt Appetite and Hypertension.Circulation · 2016Article
- Fetal brain 11β-hydroxysteroid dehydrogenase type 2 selectively determines programming of adult depressive-like behaviors and cognitive function, but not anxiety behaviors in male mice.Psychoneuroendocrinology · 2015Article
- Relationship between 11β-HSD2 mRNA and insulin sensitivity in term small-for-gestational age neonates after birth.International journal of clinical and experimental pathology · 2015Article
- Gestational cortisol and social play shape development of marmosets' HPA functioning and behavioral responses to stressors.Developmental psychobiology · 2014Article
- Steroids and injury to the developing brain: net harm or net benefit?Clinics in perinatology · 2014Review
- Article
- Mineralocorticoid-induced sodium appetite and renal salt retention: evidence for common signaling and effector mechanisms.Nephron. Physiology · 2014Review
- 11β-hydroxysteroid dehydrogenases: intracellular gate-keepers of tissue glucocorticoid action.Physiological reviews · 2013Review
- Glucocorticoid treatment of MCMV infected newborn mice attenuates CNS inflammation and limits deficits in cerebellar development.PLoS pathogens · 2013Article
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
Abstract
11beta-Hydroxysteroid dehydrogenase type 2 is a glucocorticoid metabolizing enzyme that catalyzes rapid inactivation of corticosterone and cortisol to inert 11-keto derivatives. As 11beta-hydroxysteroid dehydrogenase type 2 is highly expressed in the developing brain, but not in the adult CNS, we hypothesized that it may represent a protective barrier to the deleterious actions of corticosteroids on proliferating cells. To test this hypothesis we have investigated the development and growth of the cerebellum in neonatal C57BL/6 mice and mice lacking 11beta-hydroxysteroid dehydrogenase type 2 (-/-). 11beta-Hydroxysteroid dehydrogenase type 2-/- mice had consistently lower body weight throughout the neonatal period, coupled with a smaller brain size although this was normalized when corrected for body weight. The cerebellar size was smaller in 11beta-hydroxysteroid dehydrogenase type 2-/- mice, due to decreases in size of both the molecular and internal granule layers. When exogenous corticosterone was administered to the pups between postnatal days 4 and 13, 11beta-hydroxysteroid dehydrogenase type 2(-/-) mice were more sensitive, showing further inhibition of cerebellar growth while the wildtype mice were not affected. Upon withdrawal of exogenous steroid, there was a rebound growth spurt so that at day 21 postnatally, the cerebellar size in 11beta-hydroxysteroid dehydrogenase type 2-/- mice was similar to untreated mice of the same genotype. Furthermore, 11beta-hydroxysteroid dehydrogenase type 2-/- mice had a delay in the attainment of neurodevelopmental landmarks such as negative geotaxis and eye opening. We therefore suggest that 11beta-hydroxysteroid dehydrogenase type 2 acts as to protect the developing nervous system from the deleterious consequences of glucocorticoid overexposure.
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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.