Neurodegeneration in the thalamus following neonatal hypoxia-ischemia is programmed cell death

Frances Northington, Donna M. Ferriero, Lee J Martin

Research output: Contribution to journalArticle

Abstract

We studied neuronal cell body, axonal, and terminal degeneration in brains from 7-day-old rat pups recovered for 0, 1.5, 3, 6, 24, 48, 72 h, and 6 days following hypoxia-ischemia and identified proteins involved in the delayed neurodegeneration in the thalamus. We found that injury is biphasic with initial necrosis in the ipsilateral forebrain by 3 h following hypoxia-ischemia, in contrast to more delayed and apoptotic-like injury in the ventral-basal thalamus, brainstem, and other remote non-forebrain regions. Prior to the appearance of large numbers of apoptotic profiles in the ventral-basal thalamus, expression of Fas death receptor protein, activated forms of caspase 8 and caspase 3, and pro-apoptotic Bcl-2 proteins are increased. This manuscript combines our data on hypoxic-ischemic injury in the developing brain and presents evidence for at least two forms of neurodegeneration, namely, acute necrosis in the forebrain and delayed neurodegeneration in the thalamus, which is death-receptor-mediated programmed cell death.

Original languageEnglish (US)
Pages (from-to)186-191
Number of pages6
JournalDevelopmental Neuroscience
Volume23
Issue number3
DOIs
StatePublished - 2001

Fingerprint

Thalamus
Cell Death
Ischemia
Death Domain Receptors
Prosencephalon
Wounds and Injuries
Necrosis
CD95 Antigens
Proteins
Caspase 8
Brain
Caspase 3
Brain Stem
Hypoxia

Keywords

  • Apoptosis
  • Bax
  • Caspase
  • Cytochrome C oxidase
  • Fas death receptor
  • Mitochondria

ASJC Scopus subject areas

  • Neuroscience(all)

Cite this

Neurodegeneration in the thalamus following neonatal hypoxia-ischemia is programmed cell death. / Northington, Frances; Ferriero, Donna M.; Martin, Lee J.

In: Developmental Neuroscience, Vol. 23, No. 3, 2001, p. 186-191.

Research output: Contribution to journalArticle

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