Intermittent hypoxia induces time-dependent changes in the protein kinase B signaling pathway in the hippocampal CA1 region of the rat

Aviv Goldbart, Zixi Cheng, Kenneth R. Brittian, David Gozal

Research output: Contribution to journalArticlepeer-review

40 Scopus citations

Abstract

Intermittent hypoxia (IH) during sleep induces temporally defined increases in apoptosis within vulnerable brain regions such as the hippocampal CA1 region in rats. Protein kinase B (AKT) has emerged as major signal transduction protein underlying inhibition of apoptosis and consequent increases in cell survival. Sprague Dawley adult male rats were exposed during sleep to IH or to normoxia (RA) for periods ranging from 0 to 30 days, and expression of total and phosphorylated AKT, of forkhead family members FKHR and FKHRL1, and of glycogen synthase kinase 3β (GSK3β) was assessed. Decreases in phosphorylation occurred as early as 1 h IH exposure, reached a nadir at 6 h-3 days, and then progressively returned to baseline levels at 14-30 days. Phosphorylated AKT and GSK3β were intensely expressed and highly colocalized within neuronal cells (Neu-N positive) in the CA1 region. Thus, IH induces time-dependent biphasic changes in AKT survival pathways within the CA1 region that are temporally correlated with the initial increases and subsequent decreases in neuronal apoptosis.

Original languageEnglish
Pages (from-to)440-446
Number of pages7
JournalNeurobiology of Disease
Volume14
Issue number3
DOIs
StatePublished - 1 Jan 2003
Externally publishedYes

Keywords

  • Apoptosis
  • Forkhead transcription factors
  • Glycogen synthase kinase
  • Hippocampus
  • Intermittent hypoxia
  • Protein kinase B
  • Sleep apnea

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