RAPID AND OPPOSITE EFFECTS OF DEXAMETHASONE ON IN-VIVO AND IN-VITRO HYPOTHALAMIC SOMATOSTATIN RELEASE

We have previously reported the rapid response of hypothalamic somatos tatin (SS) neurons to acute stress. Since it is well known that glucoc orticoids (GC) are involved in neuroendocrinal stress regulation, we i nvestigate in this study the effects of acute administration of dexame thasone (Dex) on both in vivo and in vitro SS release. Freely moving a nimals received stereotaxic implant of a push-pull cannula into the me dian eminence for 10 days, and then they were perfused with artificial cerebrospinal fluid for 120-150 min. An i.p. injection of Dex (200 or 300 mu g/100 g) induced, 15-30 min later, a mean increase in SS hypot halamic output of 62.6+/-6.2% of basal secretion. By contrast, after 1 5 min incubation of hypothalamic fragments with either 10(-7) or 10(-6 ) M Dex, SS release decreased abruptly to 57.3+/-3.3% (n=16; P<0.001 c ompared with basal re lease) and 78.0+/-9.5% (n=13; P<0.05 compared wi th basal release) of basal release, respectively. Other Dex concentrat ions induced no variations, giving the dose-effect curve an abrupt ''o n-off'' effect. The inhibitory effect was blocked by picrotoxin (10(-4 ) M) and was immediately reversed when Dex was removed from the medium . Specificity was tested by using another steroid, estradiol, and anot her tissue, cortex. The rapid action of GC whatever the model used and in particular the blocking in vitro effect of picrotoxin could sugges t that GCs act at the level of the membrane and could operate physiolo gically in response to stress. In addition, the opposite in vivo and i n vitro effects on SS release would indicate that GCs exert two differ ent controls on SS neurons.