PATHOPHYSIOLOGY AND TREATMENT OF STRIATONIGRAL ISCHEMIC INJURY

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Behavioral, magnetic resonance imaging and histological studies were performed on the striatonigral system of rats with unilateral reversible middle cerebral occlusion, and following results were obtained.(1) The rats subjected to 15 to 120 minutes ischemia exhibited the ipsiversive rotational behavior elicited by systemic administration of dopamine receptor agonist apomorphine.(2) magnetic resonance imaging study showed that T2 high-signal-intensity aresa appeared earlier in the ipsilateral striatum and cortex and the size increased with the duration of ischemia. Disruption of the blood-cerebrospinal fluid barrier following transient ischemia was demonstrated by MR imaging using Gd-DTPA enhancement.(3) Histologically, the ipsilateral striatum of the rats showed a subdivisional ischemic injury. The striatal lesions having a cell type-specific injury were located in the dorsolateral portion of the rostral striatum. There was also a marked depletion of striatonigral afferents in the lateral portion of the substantia nigra pars reticulata. Activation of the microglia was noted in the ipsilateral cortex and the substantia nigra following ischemia.(4) Immunohistochemical study in the rat with striatal ischemic lesion followed by intrastriatal grafts derived from fetal striatal peimordia demonstrated that the striatopallidal pathway was reformend by striatal projection neurons of the transplants.