Delayed histopathological neuronal damage in the substantia nigra compacta (nucleus A9) after transient forebrain ischaemia

• Published in: Neurobiology of disease Vol. 2; no. 2; pp. 119 - 127
• Main Authors: Volpe, Bruce T., Blau, Alan D., Wessel, Thomas C., Saji, Makoto
• Format: Journal Article
• Language: English
• Published: United States Elsevier Inc 01-04-1995; Elsevier
• Subjects: Analysis of Variance; Animals; delayed degeneration; ischaemia; Ischemic Attack, Transient - pathology; Neurons - pathology; Prosencephalon - blood supply; quantitative histology; Rats; Substantia Nigra - pathology; substantia nigra compacta; Time Factors; tyrosine hydroxylase immunoreactive neurones; tyrosine hydroxylase immunoreactive neurones; delayed degeneration; quantitative histology; ischaemia; substantia nigra compacta
• ISSN: 0969-9961; 1095-953X
• DOI: 10.1006/nbdi.1995.0012

Neurones in the rat substantia nigra compacta (SNC) are initially resistant to transient forebrain ischaemia in contrast to vulnerable neurones in the striatum that die within 24 h. Animals were exposed to 20 min of four vessel occlusion and killed 1 and 3 weeks after reperfusion. All ischaemic animals had striatal neurone loss. Analysis of the number of tyrosine hydroxylase immunoreactive neurones (THir) in the SNC was comparable between controls and ischaemic animals killed 1 week after reperfusion. However, there was a significant reduction in THir neurone number (24%), SNC volume (17%), and THir dendritic arborization in the substantia nigra reticulata (SNR) that occurred 3 weeks after reperfusion, despite the persistence of THir axons in the striatum. Detailed morphological analysis of areas distant from the initial ischaemic injury suggest delayed degeneration may play an important role in the brain's response to ischaemia, and may provide insights for clinical stroke treatment and management.