Proceedings of The Physiological Society

University of Bristol (2005) J Physiol 567P, PC62

Poster Communications

Effects of glucocorticoids neonatal administration upon the neuronal viability and enzymes activities in hippocampus

Clichici, Simona; Joanta, Adela; Filip, Adriana; Puica, Constantin; Rusu, Mircea; Dorofteiu, Mircea;

1. Physiology, University of Medicine and Pharmacy, Cluj-Napoca, Romania. 2. Animal Physiology, Biological Center Research, Cluj-Napoca, Romania.


High levels of glucocorticoids represent neurodegenerative factors especially in the hippocampusm which is very rich in glucocorticoid and NMDA receptors. The mechanism is not entirely understood,but it appears that, among other factors, the energetic metabolism of the cell might be involved. Experimentally, we have studied, in Wistar rats, the effects upon the viability of neurones from hippocampus, as well as upon cytochrome oxidase activity and Mg-dependent ATPase activity, occuring after the administration of glucocorticoids during the first 24 h of life. Studies were performed with 2 groups of rats, with 10 animals in each group: group I - control; group II - injected i.p. with dexamethasone (2μg/g of body weight, single dose) during the first 24 h of life. With the 2 groups, at the age of 3 days, we explored: the neuronal viability through microscopic examination in UV of the brain sections stained with acridine orange (Evenson method), the cytochrome oxidase activity (Burstone and Buttcher method) and the Mg-dependent ATPase activity (Wachstein and Meissel method). All animals were humanely killed at the end of the experiment. Our results indicate that the neonatal administration of dexamethasone determine neuronal death in hippocampus, the neuronal loss being statistically significant as compared with the control group (dexamethasone group: 6526±453 neurons, control group: 9438±323, p<0.001, a decrease of 31%). The cytochrome oxidase activity is decreased, as well as the Mg-dependent ATPase activity, emphasizing a possible implication of the mitochondrial disorders in the neuronal loss.

Where applicable, experiments conform with Society ethical requirements