STRESS HYPERGLYCEMIC RESPONSE AFTER CENTRAL AND PERIPHERAL MONO-AMINERGIC NEURONS DESTRUCTION, OR ADRENAL CATECHOLAMINES DEPRIVATION
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1982
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Abstract
Restraint stress of 60 min in unfasted non-diabetic 80%-pancreatectomized rats produced a stress diabetic response with significant glycosuria and hyperglycemia. This model was used to investigate the influence of central noradrenergic, dopaminergic, serotoninergic and peripheral noradrenergic neurons, by means of selective chemical lesion. 6-Hydroxydopamine (6-OH-DA) was used to damage noradrenergic and dopaminergic neurons and 5,6-dihydroxytryptamine for serotoninergic neurons. The sympatho-adrenal system was also studied by adrenal demedullation. Results showed that intracerebro-ventricular administration of 6-OH-DA alone, or followed by 5,6-dihydroxytryptamine, had no influence on the stress hyperglycemic response. Central and peripheral 6-OH-DA administration to intact new born rats did not modify the stress response at the adult age. The hypothalamic monoaminergic and neighboring neurons appear to have no influence in the mechanism of stress hyperglycemia. The pseudo-aggressive behavior which arose after central noradrenergic and dopaminergic lesion, returned to normal after serotoninergic neuron destruction. Bilateral adrenal-medullectomy abolished the stress hyperglycemia. Adrenal catecholamines were necessary for the production of restraint stress hyperglycemia. Among these catecholamines, adrenaline [epinephrine] is proposed as the trigger factor.