Iron accumulation in the rat basal ganglia after excitatory amino acid injections--dissociation from neuronal loss.

ABSTRACT

The current study examines in an animal model the relation of excessive iron accumulation in the basal ganglia to the pathology of Parkinsonism and Hallervoden-Spatz disease. Following a unilateral microinjection of excitatory amino acids, kainate, or quinolinate to the anterior olfactory nucleus/ventral striatal region, an increase in histochemical iron concentration was observed in the ipsilateral ventral pallidum, the islands of calleja, the globus pallidus, the entopeduncular nucleus, the ventral thalamus, and the substantia nigra pars reticulata. The iron was observed both in glia and as intensification of patches in the neuropil. In a second group of rats, after microinjection of ibotenate or quisqualate to the nucleus basalis of Meynert, iron accumulated in the ipsilateral entopeduncular nucleus and pars reticulata of substantia nigra. Increased iron accumulation, compared to that in the contralateral side, was stable for months after a single microinjection. In the basal ganglia distal from the site of EAA injection, no gross morphological changes were associated with the increased iron accumulation. The implications of these findings to the pathology of Parkinson's and Hallervorden-Spatz diseases are discussed.