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首页> 外文期刊>Neuroscience: An International Journal under the Editorial Direction of IBRO >Glutamic acid decarboxylase and GABA immunoreactivities in the cerebellar cortex of adult rat after prenatal exposure to a low concentration of carbon monoxide.
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Glutamic acid decarboxylase and GABA immunoreactivities in the cerebellar cortex of adult rat after prenatal exposure to a low concentration of carbon monoxide.

机译:产前暴露于低浓度一氧化碳后成年大鼠小脑皮质的谷氨酸脱羧酶和GABA免疫反应性。

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摘要

Glutamic acid decarboxylase and GABA immunoreactivities were qualitatively and quantitatively evaluated in the cerebellar cortex of adult rats prenatally exposed to a low concentration of carbon monoxide (75 parts per million). Carbon monoxide-exposed and control rats were perfused with modified Bouin's fluid and their cerebella were embedded in paraffin. Sections from the vermis of each cerebellum were stained with Toluidine Blue or assayed with anti-glutamic acid decarboxylase 65/67 or with anti-GABA antisera. In the Toluidine Blue-stained sections, no differences were observed in the microscopic structure of the cerebellar cortex between carbon monoxide-exposed rats and controls. The distribution patterns of glutamic acid decarboxylase and GABA immunoreactivities in the cerebellar cortex of the treated animals were qualitatively comparable to those of the controls, and in accordance with previous descriptions of glutamic acid decarboxylase and GABA immunoreactivities in the rat cerebellar cortex. However, quantitative analyses demonstrated a significant reduction of immunoreactivities to both substances in the exposed rats in comparison with the controls. The reduction regarded: in the molecular layer, the number of glutamic acid decarboxylase/GABA-immunoreactive neuronal bodies and of axon terminals and the area they covered; in the Purkinje neuron layer, the number and the area covered by glutamic acid decarboxylase/GABA immunoreactive axon terminals. The differences detected in the prenatally exposed adult rats could be due to carbon monoxide-induced impairment of the differentiation of cerebellar GABA synthesizing neurons. A consequently diminished synthesis of GABA might account for some behavioral disorders detected in adult rats submitted to the same experimental procedure.
机译:在产前暴露于低浓度一氧化碳(百万分之75)的成年大鼠的小脑皮质中,定性和定量地评估了谷氨酸脱羧酶和GABA的免疫反应性。一氧化碳暴露和对照组大鼠灌输改良的Bouin液,小脑包埋在石蜡中。用甲苯胺蓝对每个小脑的the部进行染色,或用抗谷氨酸脱羧酶65/67或抗GABA抗血清进行分析。在甲苯胺蓝染色的切片中,一氧化碳暴露的大鼠和对照组之间小脑皮质的微观结构没有观察到差异。在处理后的小脑皮质中,谷氨酸脱羧酶和GABA免疫反应性的分布模式与对照在质上可比,并且根据大鼠小脑皮质中谷氨酸脱羧酶和GABA免疫反应性的先前描述。但是,定量分析表明,与对照组相比,暴露大鼠中两种物质的免疫反应性均显着降低。减少的原因是:在分子层中,谷氨酸脱羧酶/ GABA免疫反应性神经元体和轴突末端的数目及其覆盖的面积;在浦肯野神经元层中,谷氨酸脱羧酶/ GABA免疫反应性轴突末端的数目和面积。在产前暴露的成年大鼠中检测到的差异可能是由于一氧化碳诱导的小脑GABA合成神经元分化的损害。因此,GABA的合成减少可能是在接受相同实验程序的成年大鼠中检测到的某些行为障碍的原因。

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