Literature DB >> 16112480

Glutamic acid decarboxylase and GABA immunoreactivities in the cerebellar cortex of adult rat after prenatal exposure to a low concentration of carbon monoxide.

V Benagiano1, L Lorusso, A Coluccia, A Tarullo, P Flace, F Girolamo, L Bosco, R Cagiano, G Ambrosi.   

Abstract

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.

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Year:  2005        PMID: 16112480     DOI: 10.1016/j.neuroscience.2005.06.058

Source DB:  PubMed          Journal:  Neuroscience        ISSN: 0306-4522            Impact factor:   3.590


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