Dexmedetomidine protects against glucocorticoid induced progenitor cell apoptosis in neonatal mouse cerebellum

Objectives: Glucocorticoids (GCs) are used to improve respiratory mechanics in preterm infants despite clinical evidence linking neonatal GC therapy to cerebellar pathology. In developing mouse cerebellum, the GC dexamethasone (DEX) causes rapid GC-induced neural progenitor cell apoptosis (GINA). Fo...

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Bibliographic Details
Published in:The journal of maternal-fetal & neonatal medicine 2017-09, Vol.30 (18), p.2156-2162
Main Authors: O'Connor, Shawn David, Cabrera, Omar Hoseá, Dougherty, Joseph D., Singh, Sukrit, Swiney, Brant Stephen, Salinas-Contreras, Patricia, Farber, Nuri Bradford, Noguchi, Kevin Kiyoshi
Format: Article
Language:English
Subjects:
Animals
Animals, Newborn
Apoptosis - drug effects
Cell Culture Techniques
cerebellum
Cerebellum - drug effects
dexamethasone
Dexmedetomidine
Dexmedetomidine - pharmacology
Disease Models, Animal
Dose-Response Relationship, Drug
glucocorticoid
Glucocorticoids - adverse effects
Mice
Mice, Inbred ICR
neural progenitor cell
neuroprotection
Neuroprotective Agents - pharmacology
Random Allocation
Respiration - drug effects
Signal Transduction - drug effects
Stem Cells - drug effects
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Summary:Objectives: Glucocorticoids (GCs) are used to improve respiratory mechanics in preterm infants despite clinical evidence linking neonatal GC therapy to cerebellar pathology. In developing mouse cerebellum, the GC dexamethasone (DEX) causes rapid GC-induced neural progenitor cell apoptosis (GINA). Focusing on pharmacological neuroprotection strategies, we investigated whether dexmedetomidine (DMT) protects against GINA. Methods: Neonatal mice were pretreated with DMT prior to DEX challenge. Additionally, we tested clonidine and yohimbine in vivo to determine mechanism of DMT neuroprotection. For in vitro studies, cerebellar neural progenitor cells were pretreated with DMT before DEX challenge. Results: In vivo, DMT attenuated GINA at 1 μg/kg and above, p 
ISSN:1476-7058
1476-4954
1476-4954
DOI:10.1080/14767058.2016.1241763