Delayed neuronal damage following focal ischemic injury in stroke-prone spontaneously hypertensive rats

We detected the delayed accumulation of 45Ca in the lateral part of the striatum 3 days after distal middle cerebral artery (MCA) occlusion in stroke-prone spontaneously hypertensive rats (SHRSP). However, the mechanism of delayed neuronal damage in the striatum, which is not supplied by the occluded MCA, remains unknown. The aim of this study was to evaluate whether the delayed damage involves alterations in the extracellular release of neurotransmitter monoamines and amino acids. Chronological changes in the distribution of neuronal damage were determined by 45Ca autoradiography. The microdialysis probes were inserted into either the medial or lateral part of the striatum. The dialysate content of monoamines, their metabolites and amino acids was determined by analytical techniques. 45Ca accumulation was detected only in the cortex and corpus callosum by 24 hours postischemia and extended to the pyramidal tract, thalamus and lateral portion of the striatum by 3 days. A 3-fold increase in glutamate content, and a 2-fold increase in dopamine content were observed only in the lateral part of the striatum following ischemia. The results suggest that excessive release of glutamate and dopamine is related to delayed neuronal damage that occurs in the lateral part of the striatum in this ischemic model.