Shuaib A, Ijaz S, Kalra J, Code W
Department of Medicine, College of Medicine, University of Saskatchewan, Saskatoon, Canada.
Brain Res. 1992 Mar 6;574(1-2):120-4. doi: 10.1016/0006-8993(92)90807-l.
Repetitive cerebral ischemia results in severe neuronal damage in multiple regions of the brain including the hippocampus, striatum, thalamus, medial geniculate nucleus and the substantia nigra reticulata (SNr). We postulated that the damage in the SNr was delayed, resulting from a loss of striatal inhibitory input. We used the gerbil model of repetitive ischemia (3 min times 2 and 3 min times 3) to evaluate the extent of neuronal damage at 2, 3, 5 and 7 days after the ischemic insult. Silver degeneration stain was used for histological evaluation. Our results indicate that damage in the SNr begins after 48 h and is maximum at 7 days. This delay in onset of damage offers a window for pharmacological protection.