Benagiano V, Lorusso L, Coluccia A, Tarullo A, Flace P, Girolamo F, Bosco L, Cagiano R, Ambrosi G
Department of Human Anatomy and Histology, Medical Faculty, University of Bari, Policlinico, Piazza Giulio Cesare, 70124 Bari, Italy.
Neuroscience. 2005;135(3):897-905. doi: 10.1016/j.neuroscience.2005.06.058. Epub 2005 Aug 19.
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.
对产前暴露于低浓度一氧化碳(百万分之75)的成年大鼠小脑皮质中的谷氨酸脱羧酶和GABA免疫反应性进行了定性和定量评估。将暴露于一氧化碳的大鼠和对照大鼠用改良的Bouin氏液灌注,其小脑嵌入石蜡中。每个小脑蚓部的切片用甲苯胺蓝染色或用抗谷氨酸脱羧酶65/67或抗GABA抗血清进行检测。在甲苯胺蓝染色的切片中,暴露于一氧化碳的大鼠和对照大鼠的小脑皮质微观结构未观察到差异。处理动物小脑皮质中谷氨酸脱羧酶和GABA免疫反应性的分布模式在定性上与对照相当,并且与先前对大鼠小脑皮质中谷氨酸脱羧酶和GABA免疫反应性的描述一致。然而,定量分析表明,与对照相比,暴露大鼠中这两种物质的免疫反应性显著降低。降低涉及:在分子层中,谷氨酸脱羧酶/GABA免疫反应性神经元体、轴突终末的数量及其覆盖的面积;在浦肯野神经元层中,谷氨酸脱羧酶/GABA免疫反应性轴突终末的数量及其覆盖的面积。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合成神经元分化受损。因此,GABA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一些行为障碍的原因。