The Role of Growth Retardation in Lasting Effects of Neonatal Dexamethasone Treatment on Hippocampal Synaptic Function
dc.contributor.author | Wang, Yu-Chen | |
dc.contributor.author | Huang, Chiung-Chun | |
dc.contributor.author | Hsu, Kuei-Sen | |
dc.contributor.editor | Mei, Lin | |
dc.date.accessioned | 2012-10-26T16:26:50Z | |
dc.date.available | 2012-10-26T16:26:50Z | |
dc.date.issued | 2010-09-21 | en_US |
dc.identifier.citation | PLoS One. 2010 Sep 21; 5(9):e12806 | en_US |
dc.identifier.issn | 1932-6203 | en_US |
dc.identifier.pmid | 20877626 | en_US |
dc.identifier.doi | 10.1371/journal.pone.0012806 | en_US |
dc.identifier.uri | http://hdl.handle.net/10675.2/596 | |
dc.description.abstract | null | |
dc.description.abstract | Background: Dexamethasone (DEX), a synthetic glucocorticoid, is commonly used to prevent or lessen the morbidity of chronic lung disease in preterm infants. However, evidence is now increasing that this clinical practice negatively affects somatic growth and may result in long-lasting neurodevelopmental deficits. We therefore hypothesized that supporting normal somatic growth may overcome the lasting adverse effects of neonatal DEX treatment on hippocampal function. | |
dc.description.abstract | Methodology/Principal Findings: To test this hypothesis, we developed a rat model using a schedule of tapering doses of DEX similar to that used in premature infants and examined whether the lasting influence of neonatal DEX treatment on hippocampal synaptic plasticity and memory performance are correlated with the deficits in somatic growth. We confirmed that neonatal DEX treatment switched the direction of synaptic plasticity in hippocampal CA1 region, favoring low-frequency stimulation- and group I metabotropic glutamate receptor agonist (S)-3,5,-dihydroxyphenylglycine | |
dc.description.abstract | Conclusion/Significance: Our results demonstrate that growth retardation plays a crucial role in DEX-induced long-lasting influence of hippocampal function. Our findings suggest that therapeutic strategies designed to support normal development and somatic growth may exert beneficial effects to reduce lasting adverse effects following neonatal DEX treatment. | |
dc.rights | Wang et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. | en_US |
dc.subject | Research Article | en_US |
dc.subject | Neurological Disorders/Cognitive Neurology and Dementia | en_US |
dc.subject | Neurological Disorders/Developmental and Pediatric Neurology | en_US |
dc.subject | Neurological Disorders/Neuropharmacology | en_US |
dc.subject.mesh | Animals | en_US |
dc.subject.mesh | Child Development | en_US |
dc.subject.mesh | Dexamethasone | en_US |
dc.subject.mesh | Disease Models, Animal | en_US |
dc.subject.mesh | Female | en_US |
dc.subject.mesh | Hippocampus | en_US |
dc.subject.mesh | Humans | en_US |
dc.subject.mesh | Infant | en_US |
dc.subject.mesh | Long-Term Synaptic Depression | en_US |
dc.subject.mesh | Male | en_US |
dc.subject.mesh | Neuronal Plasticity | en_US |
dc.subject.mesh | Rats | en_US |
dc.subject.mesh | Rats, Sprague-Dawley | en_US |
dc.subject.mesh | Time | en_US |
dc.title | The Role of Growth Retardation in Lasting Effects of Neonatal Dexamethasone Treatment on Hippocampal Synaptic Function | en_US |
dc.type | Article | en_US |
dc.identifier.pmcid | PMC2943478 | en_US |
dc.contributor.corporatename | Department of Neurology | |
dc.contributor.corporatename | College of Graduate Studies | |
refterms.dateFOA | 2019-04-09T22:30:44Z | |
html.description.abstract | null | |
html.description.abstract | Background: Dexamethasone (DEX), a synthetic glucocorticoid, is commonly used to prevent or lessen the morbidity of chronic lung disease in preterm infants. However, evidence is now increasing that this clinical practice negatively affects somatic growth and may result in long-lasting neurodevelopmental deficits. We therefore hypothesized that supporting normal somatic growth may overcome the lasting adverse effects of neonatal DEX treatment on hippocampal function. | |
html.description.abstract | Methodology/Principal Findings: To test this hypothesis, we developed a rat model using a schedule of tapering doses of DEX similar to that used in premature infants and examined whether the lasting influence of neonatal DEX treatment on hippocampal synaptic plasticity and memory performance are correlated with the deficits in somatic growth. We confirmed that neonatal DEX treatment switched the direction of synaptic plasticity in hippocampal CA1 region, favoring low-frequency stimulation- and group I metabotropic glutamate receptor agonist (S)-3,5,-dihydroxyphenylglycine | |
html.description.abstract | Conclusion/Significance: Our results demonstrate that growth retardation plays a crucial role in DEX-induced long-lasting influence of hippocampal function. Our findings suggest that therapeutic strategies designed to support normal development and somatic growth may exert beneficial effects to reduce lasting adverse effects following neonatal DEX treatment. |