Sequential development of reversible and irreversible neuronal damage following cerebral ischemia

Carol Petito, W. A. Pulsinelli

Research output: Contribution to journalArticle

112 Citations (Scopus)

Abstract

The ultrastructure of reversibly injured cortical neurons and irreversibly injured striatal neurons was studied at 3, 15, 30, and 120 minutes (min) and 24 hours (h) following severe cerebral ischemia produced in rats by permanent occlusion of the vertebral arteries and 30 min occlusion of the carotid arteries. Animals meeting the established criterion of unresponsiveness had widespread neuronal death in the dorsolateral striatum, but no permanent damage in the paramedian cortex. Reversible mitochondrial swelling at three min was followed by dissocation of polyribosomes, decrease in rough endoplasmic reticulum (RER) profiles, and transformation of Golgi apparatus into large clusters of small vesicles by 120 min after reperfusion, followed by progressive cell shrinkage and ischemic cell change. Approximately 10-15% of striatal neurons contained cytoplasmic membranous whorls, some continuous with the plasma membrane. The results suggest that structural abnormalities in the Golgi apparatus and in plasma membranes may participate in functional changes critical to irreversible neuronal injury following cerebral ischemia.

Original languageEnglish
Pages (from-to)141-153
Number of pages13
JournalJournal of Neuropathology and Experimental Neurology
Volume43
Issue number2
StatePublished - Jan 1 1984
Externally publishedYes

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Brain Ischemia
Corpus Striatum
Golgi Apparatus
Neurons
Cell Membrane
Mitochondrial Swelling
Polyribosomes
Vertebral Artery
Rough Endoplasmic Reticulum
Carotid Arteries
Reperfusion
Wounds and Injuries

ASJC Scopus subject areas

  • Pathology and Forensic Medicine
  • Neuroscience(all)

Cite this

Sequential development of reversible and irreversible neuronal damage following cerebral ischemia. / Petito, Carol; Pulsinelli, W. A.

In: Journal of Neuropathology and Experimental Neurology, Vol. 43, No. 2, 01.01.1984, p. 141-153.

Research output: Contribution to journalArticle

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