Glucocorticoid Induced Cerebellar Toxicity in the Developing Neonate: Implications for Glucocorticoid Therapy during Bronchopulmonary Dysplasia
Prematurely born infants commonly suffer respiratory dysfunction due to the immature state of their lungs. As a result, clinicians often administer glucocorticoid (GC) therapy to accelerate lung maturation and reduce inflammation. Unfortunately, several studies have found GC therapy can also produce...
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| Format: | Article |
| Language: | English |
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MDPI AG
2014-01-01
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| Series: | Cells |
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| Online Access: | http://www.mdpi.com/2073-4409/3/1/36 |
| _version_ | 1797727474251988992 |
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| author | Kevin K. Noguchi |
| author_facet | Kevin K. Noguchi |
| author_sort | Kevin K. Noguchi |
| collection | DOAJ |
| description | Prematurely born infants commonly suffer respiratory dysfunction due to the immature state of their lungs. As a result, clinicians often administer glucocorticoid (GC) therapy to accelerate lung maturation and reduce inflammation. Unfortunately, several studies have found GC therapy can also produce neuromotor/cognitive deficits and selectively stunt the cerebellum. However, despite its continued use, relatively little is known about how exposure to this hormone might produce neurodevelopmental deficits. In this review, we use rodent and human research to provide evidence that GC therapy may disrupt cerebellar development through the rapid induction of apoptosis in the cerebellar external granule layer (EGL). The EGL is a transient proliferative region responsible for the production of over 90% of the neurons in the cerebellum. During normal development, endogenous GC stimulation is thought to selectively signal the elimination of the EGL once production of new neurons is complete. As a result, GC therapy may precociously eliminate the EGL before it can produce enough neurons for normal cerebellar function. It is hoped that this review may provide information for future clinical research in addition to translational guidance for the safer use of GC therapy. |
| first_indexed | 2024-03-12T11:00:15Z |
| format | Article |
| id | doaj.art-1b260f2c595a435eb41edc5fe32c199c |
| institution | Directory Open Access Journal |
| issn | 2073-4409 |
| language | English |
| last_indexed | 2024-03-12T11:00:15Z |
| publishDate | 2014-01-01 |
| publisher | MDPI AG |
| record_format | Article |
| series | Cells |
| spelling | doaj.art-1b260f2c595a435eb41edc5fe32c199c2023-09-02T05:45:19ZengMDPI AGCells2073-44092014-01-0131365210.3390/cells3010036cells3010036Glucocorticoid Induced Cerebellar Toxicity in the Developing Neonate: Implications for Glucocorticoid Therapy during Bronchopulmonary DysplasiaKevin K. Noguchi0Department of Psychiatry, School of Medicine, Washington University in St. Louis, 660 South Euclid, Box #8134, St. Louis, MO 63110, USAPrematurely born infants commonly suffer respiratory dysfunction due to the immature state of their lungs. As a result, clinicians often administer glucocorticoid (GC) therapy to accelerate lung maturation and reduce inflammation. Unfortunately, several studies have found GC therapy can also produce neuromotor/cognitive deficits and selectively stunt the cerebellum. However, despite its continued use, relatively little is known about how exposure to this hormone might produce neurodevelopmental deficits. In this review, we use rodent and human research to provide evidence that GC therapy may disrupt cerebellar development through the rapid induction of apoptosis in the cerebellar external granule layer (EGL). The EGL is a transient proliferative region responsible for the production of over 90% of the neurons in the cerebellum. During normal development, endogenous GC stimulation is thought to selectively signal the elimination of the EGL once production of new neurons is complete. As a result, GC therapy may precociously eliminate the EGL before it can produce enough neurons for normal cerebellar function. It is hoped that this review may provide information for future clinical research in addition to translational guidance for the safer use of GC therapy.http://www.mdpi.com/2073-4409/3/1/36bronchopulmonary dysplasiadexamethasonebetamethasonehydrocortisonecerebellum11β-Hydroxysteroid Dehydrogenase Type IIcerebellumapoptosisexternal granule layerneural progenitor cell |
| spellingShingle | Kevin K. Noguchi Glucocorticoid Induced Cerebellar Toxicity in the Developing Neonate: Implications for Glucocorticoid Therapy during Bronchopulmonary Dysplasia Cells bronchopulmonary dysplasia dexamethasone betamethasone hydrocortisone cerebellum 11β-Hydroxysteroid Dehydrogenase Type II cerebellum apoptosis external granule layer neural progenitor cell |
| title | Glucocorticoid Induced Cerebellar Toxicity in the Developing Neonate: Implications for Glucocorticoid Therapy during Bronchopulmonary Dysplasia |
| title_full | Glucocorticoid Induced Cerebellar Toxicity in the Developing Neonate: Implications for Glucocorticoid Therapy during Bronchopulmonary Dysplasia |
| title_fullStr | Glucocorticoid Induced Cerebellar Toxicity in the Developing Neonate: Implications for Glucocorticoid Therapy during Bronchopulmonary Dysplasia |
| title_full_unstemmed | Glucocorticoid Induced Cerebellar Toxicity in the Developing Neonate: Implications for Glucocorticoid Therapy during Bronchopulmonary Dysplasia |
| title_short | Glucocorticoid Induced Cerebellar Toxicity in the Developing Neonate: Implications for Glucocorticoid Therapy during Bronchopulmonary Dysplasia |
| title_sort | glucocorticoid induced cerebellar toxicity in the developing neonate implications for glucocorticoid therapy during bronchopulmonary dysplasia |
| topic | bronchopulmonary dysplasia dexamethasone betamethasone hydrocortisone cerebellum 11β-Hydroxysteroid Dehydrogenase Type II cerebellum apoptosis external granule layer neural progenitor cell |
| url | http://www.mdpi.com/2073-4409/3/1/36 |
| work_keys_str_mv | AT kevinknoguchi glucocorticoidinducedcerebellartoxicityinthedevelopingneonateimplicationsforglucocorticoidtherapyduringbronchopulmonarydysplasia |