Delayed histopathological neuronal damage in the substantia nigra compacta (nucleus A9) after transient forebrain ischaemia.
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.
Volpe
B T
BT
Department of Neurology and Neuroscience, Cornell University Medical Centre at the Winifred Masterson Burke Research Institute, White Plains, New York 10605, USA.
Blau
A D
AD
Wessel
T C
TC
Saji
M
M
D000704:Analysis of Variance; D000818:Animals; D002546:Ischemic Attack, Transient / Q000473:pathology*; D009474:Neurons / Q000473:pathology*; D016548:Prosencephalon / Q000098:blood supply*; D051381:Rats; D013378:Substantia Nigra / Q000473:pathology*; D013997:Time Factors