Glutamate dehydrogenase in astrocytes of the rat dentate gyrus following lesion of the entorhinal cortex.
Applying quantitative microscopic histochemistry, the activity of the mitochondrial glutamate dehydrogenase which is localized in astrocytes was determined in the molecular layer of the dentate gyrus of the rat hippocampus. This hippocampal region contains the important terminations of the glutamatergic perforant path. For comparison, determinations of the mitochondrial succinate dehydrogenase were performed, which is localized preferentially in terminals and dendrites. Two age groups of animals were examined: young adults (three months old) and aged subjects (24 months old). Both age groups were divided into controls, and animals killed three, 21 and 90 days following unilateral electrolytic lesion of the entorhinal cortex. The post-lesional shrinkage of the terminal field of the perforant path, ipsilateral to the lesion side, was determined and considered in the evaluation of enzymatic data. Statistic analysis revealed that ipsilateral to the lesion side there was a significant decrease of glutamate and succinate dehydrogenase activities in the terminal field of the perforant path three, 21 and 90 days following lesion. It is reasonable to assume that the decrease of succinate dehydrogenase activity (50-60%) was caused by the loss of mitochondria localized in degenerating terminals, whereas the decrease of glutamate dehydrogenase activity (20-30%) was related to the decrease of glutamatergic transmission following lesion. In the terminal field of the perforant path contralateral to the lesion side both significant increases and decreases of enzyme activities were measured following lesion. From these results it is concluded that the hippocampus contralateral to the lesion side cannot be considered as an appropriate intraindividual control. The comparison between young and aged animals showed no differences in the demonstration of glutamate dehydrogenase and only restricted differences in the activity level of succinate dehydrogenase post-lesion. Therefore, it is reasonable to assume that the post-lesional reactivity of the enzymes studied was very similar in both age groups.
Kugler
P
P
Institute of Anatomy, University of Würzburg, Germany.
Weeger
T
T
Horváth
E
E
D000367:Age Factors; D000818:Animals; D001253:Astrocytes / Q000201:enzymology*; D002529:Cerebellar Nuclei / Q000201:enzymology*; D018728:Entorhinal Cortex / Q000502:physiology*; D005969:Glutamate Dehydrogenase / Q000378:metabolism*; D006624:Hippocampus / Q000502:physiology; D008297:Male; D051381:Rats; D017208:Rats, Wistar; D013385:Succinate Dehydrogenase / Q000378:metabolism; D013997:Time Factors
D013385:Succinate Dehydrogenase; D005969:Glutamate Dehydrogenase