[Histopathological alteration of the central nervous system in rats, following long-term administration of manganese chloride--relation to the activity of the brain tyrosine hydroxylase].

Chronic manganese poisoning is characterized by mental and extrapyramidal disturbances. Parkinsonism-dementia complex (PD) on Guam is also manifested by progressive extrapyramidal syndrome and dementia. In PD, the reduced activities of catecholamine synthesizing enzymes in the brain has been demonstrated. On the other hand, the soil and water in Guam are rich in manganese, and one of the possible etiologic factors is trace element dysmetabolism in PD. The purpose of this paper is to clarify the effect of chronic manganese loading on the central nervous system. Manganese chloride (10 mg/ml of demineralized and distilled water) was administrated orally to Wistar female rats weighing 80-110 g. Six and 12 months after the administration, manganese loaded and control rats were sacrificed by perfusion for histological studies and by decapitation for the assay of tyrosine hydroxylase (TH) activity. The striatum, globus pallidus and substantia nigra were examined with electron microscopy. The brain for TH assay was dissected into four parts as the striatum, midbrain-thalamus, pons-medulla oblongata, and hypothalamus. Ultrastructural changes were overwhelmingly detected in the zona reticulata of the substantia nigra at 12 months. These changes were mainly composed of alterations of the postsynapse and neuronal soma--shrunken and electron dense dendrites accumulated degenerating materials and so-called simple atrophy of the neuron. Alterations in the presynapse were extremely milder than those in the postsynapse and neuron. At both 6 and 12 months, no significant changes in the striatum and globus pallidus were detected except for irregular windings of the plasma membrane in the axon terminal of the globus pallidus at 12 months.(ABSTRACT TRUNCATED AT 250 WORDS)