The Role of Growth Retardation in Lasting Effects of Neonatal Dexamethasone Treatment on Hippocampal Synaptic Function

Hdl Handle:
http://hdl.handle.net/10675.2/596
Title:
The Role of Growth Retardation in Lasting Effects of Neonatal Dexamethasone Treatment on Hippocampal Synaptic Function
Authors:
Wang, Yu-Chen; Huang, Chiung-Chun; Hsu, Kuei-Sen ( 0000-0002-3498-5157 )
Abstract:
null; 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.; 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; 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.
Editors:
Mei, Lin
Citation:
PLoS One. 2010 Sep 21; 5(9):e12806
Issue Date:
21-Sep-2010
URI:
http://hdl.handle.net/10675.2/596
DOI:
10.1371/journal.pone.0012806
PubMed ID:
20877626
PubMed Central ID:
PMC2943478
Type:
Article
ISSN:
1932-6203
Appears in Collections:
Department of Neurology: Faculty Research and Presentations

Full metadata record

DC FieldValue Language
dc.contributor.authorWang, Yu-Chenen_US
dc.contributor.authorHuang, Chiung-Chunen_US
dc.contributor.authorHsu, Kuei-Senen_US
dc.contributor.editorMei, Lin-
dc.date.accessioned2012-10-26T16:26:50Z-
dc.date.available2012-10-26T16:26:50Z-
dc.date.issued2010-09-21en_US
dc.identifier.citationPLoS One. 2010 Sep 21; 5(9):e12806en_US
dc.identifier.issn1932-6203en_US
dc.identifier.pmid20877626en_US
dc.identifier.doi10.1371/journal.pone.0012806en_US
dc.identifier.urihttp://hdl.handle.net/10675.2/596-
dc.description.abstractnullen_US
dc.description.abstractBackground: 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.en_US
dc.description.abstractMethodology/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,-dihydroxyphenylglycineen_US
dc.description.abstractConclusion/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.en_US
dc.rightsWang 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.subjectResearch Articleen_US
dc.subjectNeurological Disorders/Cognitive Neurology and Dementiaen_US
dc.subjectNeurological Disorders/Developmental and Pediatric Neurologyen_US
dc.subjectNeurological Disorders/Neuropharmacologyen_US
dc.subject.meshAnimalsen_US
dc.subject.meshChild Developmenten_US
dc.subject.meshDexamethasoneen_US
dc.subject.meshDisease Models, Animalen_US
dc.subject.meshFemaleen_US
dc.subject.meshHippocampusen_US
dc.subject.meshHumansen_US
dc.subject.meshInfanten_US
dc.subject.meshLong-Term Synaptic Depressionen_US
dc.subject.meshMaleen_US
dc.subject.meshNeuronal Plasticityen_US
dc.subject.meshRatsen_US
dc.subject.meshRats, Sprague-Dawleyen_US
dc.subject.meshTimeen_US
dc.titleThe Role of Growth Retardation in Lasting Effects of Neonatal Dexamethasone Treatment on Hippocampal Synaptic Functionen_US
dc.typeArticleen_US
dc.identifier.pmcidPMC2943478en_US
dc.contributor.corporatenameDepartment of Neurology-
dc.contributor.corporatenameCollege of Graduate Studies-

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