Browsing by Author "TapiaArancibia, L"

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    Rapid and opposite effects of dexamethasone on in vivo and in vitro hypothalamic somatostatin release
    (1997) Estupina, C; Belmar, J; TapiaArancibia, L; Astier, H; Arancibia, S
    We have previously reported the rapid response of hypothalamic somatostatin (SS) neurons to acute stress. Since it is well known that glucocorticoids (GC) are involved in neuroendocrinal stress regulation, we investigate in this study the effects of acute administration of dexamethasone (Dex) on both in vivo and in vitro SS release. Freely moving animals received stereotaxic implant of a push-pull cannula into the median 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 hypothalamic output of 62.6+/-6.2% of basal secretion. By contrast, after 15 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 compared with basal re lease) and 78.0+/-9.5% (n=13; P<0.05 compared with basal release) of basal release, respectively. Other Dex concentrations induced no variations, giving the dose-effect curve an abrupt ''on-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 another tissue, cortex. The rapid action of GC whatever the model used and in particular the blocking in vitro effect of picrotoxin could suggest that GCs act at the level of the membrane and could operate physiologically in response to stress. In addition, the opposite in vivo and in vitro effects on SS release would indicate that GCs exert two different controls on SS neurons.
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    Responsiveness to depolarization of hypothalamic neurons secreting somatostatin under stress and estrous cycle conditions: Involvement of GABAergic and steroidal interactions
    (1997) Arancibia, S; Estupina, C; Pesco, J; Belmar, J; TapiaArancibia, L
    We studied the sensitivity to a depolarizing stimulus of hypothalamic fragments dissected from cycling female donor rats exposed or not to 30-min stress at 4 degrees C. The neuronal response was estimated in terms of the ability of tissue to release somatostatin when stimulated with 40 mM K+. The data showed no differences in response to K+, regardless of the ovarian cycle of the female donors, whereas tissues dissected from ovariectomized or pregnant rats responded significantly to K+. However, when donors underwent previous cold stress, significant differences were noted at all stages of the cycle, except diestrus-1, compared with control rats, We tested whether GABA and/or neuroactive steroids could be involved in this phenomenon and observed no GABA inhibition of somatostatin release in vitro, but inhibition occurred in the presence of a neuroactive steroid, THDOC, The effect of GABA in vivo on somatostatin release was estrogen dependent because bicuculline modified the total amount of somatostatin secreted in estrus but not in diestrus II, Finally, in hypothalamic primary cultures, GABA inhibition of somatostatin release was only detected when steroids were present in the media throughout culture.