Publikationsdatenbank

Modulation der zentralnervösen Regulation der Cortisolsekretion durch metabolische Einflüsse:
Glukose, Ketonkörper, freie Fettsäuren (1994)

Art

Hochschulschrift

Autor

Torabi, Morteza

Quelle

Berlin, 1994 — 116 Seiten

Kontakt

Institut für Tierschutz, Tierverhalten und Versuchstierkunde

Königsweg 67
14163 Berlin
+49 30 838 61146
tierschutz@vetmed.fu-berlin.de

Abstract / Zusammenfassung

Five nonanesthesized male Rhesus monkeys (age: 4-10 years) were used. After a 17-hour fasting period (water ad libitum) the influence of bipolar electrostimulation (platin/steel electrode, diameter: 0,25 mm) on plasmacortisol concentrations (PCC) was studied. Six electrodes were positioned in the hypothalamus and 7 electrodes in the amygdala nuclei. Furthermore, we studied the influence of metabolite infusion (glucose, B-hydroxybutyrate, free fatty acids) on PCC increases caused by electrostimulation. In additon, we studied the influence of electrostimulation on PCC increases due to insulin hypoglycemia (IHG).Metabolite infusions and IHG tests without electrostimulations were done as control.Results:There was no difference between spontaneous PCC and PCC during metabolite infusion.Insulin-induced hypoglycemia resulted in an increase in PCC.Electrostimulation in the hypothalamus led to an increase in PCC at all stimulation sites.Increases in PCC during stimulation in the amygdala varied depending on the position of the electrode. In some cases, cortisol secretion could not be stimulated.There was no difference between cortisol responses during metabolite infusion in combination with electrostimulation in the hypothalamus and amygdala nuclei and cortisol responses in insulin-induced hypoglycemia alone.Conclusion:Electrostimulation in the hypothalamus and amygdala nuclei resulted in an increase in PCC. In some cases, cortisol secretion could not be stimulated in the amygdala area.The increase of metabolite concentrations in the blood (glucose, free fatty acids, B-hydroxybutyrate) had no significant influence on the PCC increase by electrostimulation in the hypothalamus and the amygdala nuclei. Electrostimulation in the hypothalamus and amygdala nuclei had no influence on the increase in PCC caused by insulin hypoglycemia, and vice versa. The results without electrostimulation are in accordance with the conditions in humans and the findings obtained so far in Rhesus monkeys. Hence Rhesus monkeys can be used as a model for the regulation of the hypothalmopituitary-adrenocortical system in man.