engleski

CENTRAL ORIGIN OF ALTERED NOCICEPTION IN EXPERIMENTAL DIABETES MELLITUS

Diabetes mellitus in experimental animals and in man is often accompanied by altered nociception and altered responses to different analgesic drugs, which can only partially be explained by a damage to peripheral nerves due to diabetic neuropathy. An increasing number of reports describe different alterations in brain neurotransmitters in diabetes mellitus. However, given the recent studies, intracerebroventricular (i.c.v.) administration of a non-diabetogenic dose of betacytotoxic substances, alloxan or streptozotocin, produces changes in brain monoamines and their receptors similar to those observed in diabetes mellitus, indicating that part of biochemical changes in experimental diabetes might be of a central origin. In the present experiments, using the hot plate test and tail immersion test, we investigated nociception and the effect of morphine in rats that were made diabetic by alloxan or streptozotocin, or received a non-diabetogenic dose of these substances i.c.v. Independently of the route of alloxan or streptozotocin administration, i.e. were the animals diabetic or not, all treated animals showed an increased pain threshold and a reduced analgesic effect of morphine in both tests used. The effect of i.c.v. administration was somewhat smaller and reversible. Both peripheral and i.c.v. induced effects could be prevented by simultaneous treatment with glucose. These results suggest that the central nervous system might be involved in the mechanism leading to altered nociception, at least in alloxan- and streptozotocin-induced diabetes mellitus.

diabetes mellitus; nociception; brain

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