LACK OF GLUCOCORTICOIDS SUSTAINS THE STRESS-INDUCED RELEASE OF NORADRENALINE IN THE ANTERIOR HYPOTHALAMUS

The release of endogenous noradrenaline in the anterior hypothalamus w as studied with microdialysis perfusion in freely moving rats that wer e subjected to immobilization stress. Experiments were carried out in sham-adrenalectomized and adrenalectomized rats that were first given drinking water containing corticosterone for 5 days following surgery and then switched to a corticosterone-free diet the day before stress application. One group of these adrenalectomized animals was injected with dexamethasone. Basal release of noradrenaline collected in 20-min fractions was similar in the three groups of animals and averaged 24 fmol. The recovery of the probe was about 10%. In sham-adrenalectomize d rats application of 20-min immobilization stress increased noradrena line release to 310% of baseline in the sample collected during stress application. A significant increase (+ 175% of baseline) was still ob served in the next 20-min sample. Subsequent values were all identical to baseline. In adrenalectomized rats lacking exogenous corticosteron e the stress-induced release of noradrenaline was prolonged with norad renaline levels remaining elevated for 2 h after the onset of stress. The total noradrenaline release during this entire period was about 2. 5 times higher in adrenalectomized than in sham-operated rats. However , the maximal increase during the period of immobilization was not sig nificantly affected. Treatment with dexamethasone prevented the prolon ged increase in noradrenaline release but did not affect the increase during the period of stress. While glucocorticoids do not appear to af fect the increased release of NA in the anterior hypothalamus during t he period of stress, they act to limit the duration of this activation after the application of stress. Our results show that glucocorticoid s affect the stress-induced activation of the catecholaminergic system s innervating the anterior hypothalamus, i.e. the region of the parave ntricular nucleus, and suggest that glucocorticoids exert on these sys tems a homeostatic, rather than a negative feedback, regulation during their stress-induced activation.