Early-life fluoxetine exposure reduced functional deficits after hypoxic-ischemia brain injury in rat pups

Ying Chao Chang, Shun Fen Tzeng, Lung Yu, A. Min Huang, Hsueh Te Lee, Chao Ching Huang, Chien Jung Ho

Research output: Contribution to journalArticle

48 Citations (Scopus)

Abstract

Neuroplasticity after perinatal programming may allow for neuroprotection against hypoxic-ischemia (HI) at birth. The cAMP response element-binding protein (CREB) is a key mediator of stimulus-induced nuclear responses that underlie survival, memory and plasticity of nervous system. Chronic treatment of fluoxetine, a selective serotonin reuptake inhibitor, can upregulate CREB activation in the hippocampus. We examined whether fluoxetine administration before HI may protect against neonatal HI brain injury through CREB-mediated mechanisms. We found that low-dose fluoxetine pretreatment in a neonatal HI brain injury model significantly reduced functional deficits at adulthood. The neuroprotective mechanisms were associated with increased CREB phosphorylation and increased brain-derived neurotrophic factor and synapsin I mRNA expression in the hippocampus. Neurogenesis also increased because of greater precursor cell survival in the hippocampal dentate gyrus. These findings suggest that functional deficits after HI in the developing brain can be reduced by agents that enhance neural plasticity and neurogenesis through CREB activation.

Original languageEnglish
Pages (from-to)101-113
Number of pages13
JournalNeurobiology of Disease
Volume24
Issue number1
DOIs
Publication statusPublished - Oct 2006
Externally publishedYes

Fingerprint

Cyclic AMP Response Element-Binding Protein
Fluoxetine
Brain Injuries
Ischemia
Neuronal Plasticity
Neurogenesis
Hippocampus
Synapsins
Parahippocampal Gyrus
Brain-Derived Neurotrophic Factor
Dentate Gyrus
Serotonin Uptake Inhibitors
Nervous System
Cell Survival
Up-Regulation
Phosphorylation
Parturition
Messenger RNA
Brain

Keywords

  • Brain-derived neurotrophic factor
  • cAMP response element-binding protein
  • Fluoxetine
  • Hypoxic-ischemia
  • Neurogenesis
  • Newborn

ASJC Scopus subject areas

  • Neurology

Cite this

Early-life fluoxetine exposure reduced functional deficits after hypoxic-ischemia brain injury in rat pups. / Chang, Ying Chao; Tzeng, Shun Fen; Yu, Lung; Huang, A. Min; Lee, Hsueh Te; Huang, Chao Ching; Ho, Chien Jung.

In: Neurobiology of Disease, Vol. 24, No. 1, 10.2006, p. 101-113.

Research output: Contribution to journalArticle

Chang, Ying Chao ; Tzeng, Shun Fen ; Yu, Lung ; Huang, A. Min ; Lee, Hsueh Te ; Huang, Chao Ching ; Ho, Chien Jung. / Early-life fluoxetine exposure reduced functional deficits after hypoxic-ischemia brain injury in rat pups. In: Neurobiology of Disease. 2006 ; Vol. 24, No. 1. pp. 101-113.
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