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DIFFERENTIAL LOSS OF DOPAMINERGIC FIBERS IN FRONTAL CORTICAL MOTOR AREAS OF PARKINSONIAN MONKEYS l, Dept. Neurol., Juntendo Univ. Sch. Med.2, Dept. Dept. Morphol. Brain Sci., Fat. Med., Kyoto Univ. Public Health, Juntendo Univ. Sch. Med. 3, Dept. Neurobiol., Tokyo Metropol. Inst. Neurosci.4, Mol. Cell. Neurosci. Sec., Electrotech. Lab .5, Dept. Neurosurg., Gunma Univ. Sch. Med.6 JUN KOJIMA2, YOSHIO YAMAJ13, HIRONOBU TOKUNO’, ATSUSHI NAMBU4, TOSHIKAZU AKAZAWA4, MASAHIKO INASE5, MASARU MATSUMURA’, HISAMASA IMA12, MASAHIKO TAKADA’ Dopaminergic fiber distributions in multiple motor-related areas of the frontal cortex were investigated in parkinsonian monkeys. The parkinsonism-inducing drug, MPTP, was systemically administered to Japanese monkeys. Employing tyrosine hydroxylase immunohistochemistry, density levels of dopaminergic fibers in the frontal cortical motor areas were compared between normal and MPTP-treated monkeys. In normal monkeys, dense accumulations of dopaminergic fibers were observed in the medial wall motor areas, including the supplementary, presupplementary, and cingulate motor areas. Moderate levels of dopaminergic fibers were also distributed in the lateral surface motor areas, corresponding to the primary motor cortex and the dorsal and ventral divisions of the premotor cortex. In MPTP-treated monkeys, the densities of dopaminergic fibers in the medial wall motor areas were drastically reduced, whereas those in the lateral surface motor areas showed no substantial decrease.
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EFFECTS OF EPSILON TOXIN PRODUCED BY CLOSTRIDIUM PERFRINGENS ON THE RAT HIPPOCAMPUS Dept. Biology’, Basic Sports Medicine Kagawa Medical Univ., 1750-l Miki-cho 761-07, Japan2, Dept. Health and Physical Education Kagawa Univ., l-l, Saiwai-cho, Takamatsu 760, Japan3, Dept. Physiol. Kurashiki Univ. Arts and Sciences, 2640, Nishiura, Kurashiki 712, Japan4 OSAMU MIYAMOT0’*2, TETSURO NEG12, SHINICHI YAMAGAM13, YASUSHI OKADA3, TETUHIDE MURAKAM14, TOSHIFUMI ITANO’ Epsilon toxin, which is produced by Clostridium perfingens, induces fatal enterotoxemia and brain damage. It specifically accumulates in the brain after peripherally administration, and the presence of specific binding sites in synaptosomal membrane for epsilon toxin was reported. However, the precise mechanism of its action on the brain is poorly understood. We have histologically studied the effect of the toxin on the rat brain, particularly on the hippocampus, to elucidate the action mode of the toxin. The rat brains were investigated 4 h after toxin administration (25~-lOOng/kg). Hippocampal neurons were extremely vulnerable to the toxin, and MAP 2 immunoreactivity and Timm’s zinc staining were reduced by the toxin. These effects of the toxin on the hippocampal neurons were suppressed by the glutamate receptor antagonists or glutamate release inhibitor. These findings suggest that ipsilon toxin damages the hippocampus through glutamate@ system.