RESPONSIVENESS TO DEPOLARIZATION OF HYPOTHALAMIC NEURONS SECRETING SOMATOSTATIN UNDER STRESS AND ESTROUS-CYCLE CONDITIONS - INVOLVEMENT OF GABAERGIC AND STEROIDAL INTERACTIONS

We studied the sensitivity to a depolarizing stimulus of hypothalamic fragments dissected from cycling female donor rats exposed or not to 3 0-min stress at 4 degrees C. The neuronal response was estimated in te rms of the ability of tissue to release somatostatin when stimulated w ith 40 mM K+. The data showed no differences in response to K+, regard less of the ovarian cycle of the female donors, whereas tissues dissec ted from ovariectomized or pregnant rats responded significantly to K. However, when donors underwent previous cold stress, significant dif ferences were noted at all stages of the cycle, except diestrus-1, com pared with control rats, We tested whether GABA and/or neuroactive ste roids could be involved in this phenomenon and observed no GABA inhibi tion of somatostatin release in vitro, but inhibition occurred in the presence of a neuroactive steroid, THDOC, The effect of GABA in vivo o n somatostatin release was estrogen dependent because bicuculline modi fied the total amount of somatostatin secreted in estrus but not in di estrus II, Finally, in hypothalamic primary cultures, GABA inhibition of somatostatin release was only detected when steroids were present i n the media throughout culture. Our results suggest that steroid-GABA- somatostatin interactions could explain the different responses of neu rons to depolarization. (C) 1997 Wiley-Liss, Inc.