Early neurodegeneration after hypoxia-ischemia in neonatal rat is necrosis while delayed neuronal death is apoptosis

Frances J. Northington, Donna M. Ferriero, Ernest M. Graham, Richard J. Traystman, Lee J. Martin

Research output: Contribution to journalArticlepeer-review

Abstract

We used silver staining to demonstrate neuronal cell body, axonal, and terminal degeneration in brains from p7 rat pups recovered for 0, 1.5, 3, 6, 24, 48, 72 h, and 6 days following hypoxia-ischemia. We found that initial injury is evident in ipsilateral forebrain by 3 h following hypoxia-ischemia, while injury in ventral basal thalamus develops at 24 h. A secondary phase of injury occurs at 48 h in ipsilateral cortex, but not until 6 days in basal ganglia. Initial injury in striatum and cortex is necrosis, but in thalamus the neurodegeneration is primarily apoptosis. Degeneration also occurs in bilateral white matter tracts, and in synaptic terminal fields associated with apoptosis in regions remote from the primary injury. These results show that hypoxia-ischemia in the developing brain causes both early and delayed neurodegeneration in specific systems in which the morphology of neuronal death is determined by time, region, and potentially by patterns of neuronal connectivity.

Original languageEnglish (US)
Article number90371
Pages (from-to)207-219
Number of pages13
JournalNeurobiology of Disease
Volume8
Issue number2
DOIs
StatePublished - 2001

ASJC Scopus subject areas

  • Neurology

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