Delayed histologic damage and neuron death in the substantia nigra reticulata following transient forebrain ischemia depends on the extent of initial striatal injury.

Overview

Transient forebrain ischemia in normoglycemic, normotensive rodents reproducibly causes selectively vulnerable neurons in the striatum to degenerate within 24 h. Neurons in the substantia nigra reticulata (SNR) are resistant to this acute process. Histologic evidence demonstrates that the combination of acute ischemic injury to the caudate nucleus and globus pallidus is associated with delayed neuron degeneration in the SNR that matures at 3 weeks after reperfusion. Ischemia, like certain ablative neurotoxin lesions, may provoke degenerative, perhaps transneuronal events that continue to evolve long after the initial insult.