Subcutaneous administration of high doses of glutamate to rats during their first 10 days after birth produced a great reduction of GABA content and GAD activity in the adult mediobasal hypothalamus, both in male and female. In addition GABA content and GAD activity showed a slight significant decrease in female cerebellum and male striatum. Glutamate treatment was also followed by a significant increase in GABA content and GAD activity of male substantia nigra, cerebellum, hippocampus and of female olfactory bulb. No reduction in GABA-T activity was observed in different brain areas studied except in mediobasal hypothalamus. The results support the view that glutamate treatment had a direct toxic effect on GABA-ergic neurons in mediobasal hypothalamus. The changes in GAD activity observed in all areas studied may reflect the neuroendocrine changes determined by nucleus arcuate lesions.

GABA-ergic system in brain regions of glutamate-lesioned rats.

DI GIORGIO, Rosa Maria;DE LUCA, Grazia;IENTILE, Riccardo
1985-01-01

Abstract

Subcutaneous administration of high doses of glutamate to rats during their first 10 days after birth produced a great reduction of GABA content and GAD activity in the adult mediobasal hypothalamus, both in male and female. In addition GABA content and GAD activity showed a slight significant decrease in female cerebellum and male striatum. Glutamate treatment was also followed by a significant increase in GABA content and GAD activity of male substantia nigra, cerebellum, hippocampus and of female olfactory bulb. No reduction in GABA-T activity was observed in different brain areas studied except in mediobasal hypothalamus. The results support the view that glutamate treatment had a direct toxic effect on GABA-ergic neurons in mediobasal hypothalamus. The changes in GAD activity observed in all areas studied may reflect the neuroendocrine changes determined by nucleus arcuate lesions.
1985
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Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/11570/2292643
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