醋酸钴中毒大鼠脑单胺神经元的组织荧光研究。

Medical biology Pub Date : 1987-01-01
M Smiałowska, T Bugera-Piecuch, A Bal, M Smiałek
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引用次数: 0

摘要

目的是研究帕金森型锥体外系运动综合征实验动物模型脑单胺神经元的变化。对急性醋酸钴中毒大鼠轻度缺血后的神经系统体征进行了观察。组织荧光研究显示,下丘脑和中脑网状结构中儿茶酚胺荧光减少(表明胺含量减少),但在黑质和基底神经节中没有。中缝背核和中缝核的神经细胞体以及部分丘脑和视前区的神经末梢血清素荧光增强。邻近荧光切片的组织学染色未见神经元丢失和髓磷脂的病理改变。本文讨论了中毒大鼠锥体外系运动综合征中钴离子对神经元传递的干扰作用和/或多巴胺和血清素之间的失衡。
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Histofluorescence studies of monoamine neurons in the rat brain after cobaltous acetate intoxication.

The aim was to study changes in brain monoamine neurons in an experimental animal model with an extrapyramidal motor syndrome of the parkinsonian type. The neurological signs were observed in rats after acute cobaltous acetate intoxication under mild ischemic conditions. Histofluorescence studies showed a decrease in catecholamine fluorescence (which signifies a decrease in the amine content) in the hypothalamus and mesencephalic reticular formation, but not in the substantia nigra or basal ganglia. Serotonin fluorescence was increased in nerve cell bodies of the dorsal and median raphe nuclei and in nerve terminals in some thalamic and preoptic regions. Histological staining of sections adjacent to the fluorescent ones showed no neuronal loss and some pathology of myelin. The disturbing effect of cobaltous ions on the neuronal transmission, and/or the imbalance between dopamine and serotonin in the extrapyramidal motor syndrome observed in poisoned rats have been discussed.

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Growth inhibitory polypeptides in the regulation of cell proliferation. Relationship between tryptophan and serotonin concentrations in postmortem human brain. Peptides and neurotransmission in the central nervous system. GABA and affective disorders. Chemical neurotransmission in the parkinsonian brain.
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