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

研究成果: 雜誌貢獻文章同行評審

50 引文 斯高帕斯(Scopus)

摘要

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.

原文英語
頁(從 - 到)101-113
頁數13
期刊Neurobiology of Disease
24
發行號1
DOIs
出版狀態已發佈 - 10月 2006
對外發佈

ASJC Scopus subject areas

  • 神經內科

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