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A GnRH SUPERAGONIST, BUSERELIN, REDUCES GnRH RELEASE FROM THE RAT HYPOTHALAMUS IN VITRO

Single retrochiasmatic hypothalami of male rats aged 15, 30 and 50 days were studied in incubation chambers where culture medium (0.5 ml DMEM) was renewed every 7.5 min and collected for the RIA of GnRH. Using the anti-GnRH antibody RR5 provided by A. Root, no cross-reactivity was observed in the presence of buserelin concentrations < 100 nM. When the 50-day hypothalami were incubated in the presence of 50 μM veratridine, a depolarizing agent, the mean release of GnRH (± SD) was 17.8 ± 4.4 pg/ 7.5 min. From the first time buserelin (10 nM) was added, GnRH release fell to 7.5 ± 2.5 pg/7.5 min. A similar inhibition was observed at 15 and 30 days of age, persisted as long as buserelin was present and was reversible when the agonist was no more added. The spontaneous release of GnRH was significantly reduced by several buserelin concentrations between 0.01 and 10 nM. In contrast, GnRH release did not change in the presence of other analogs (leu8-GnH, picolylamide10-GnRH) or when buserelin had been previously heated at 90° for 90 min. Finally, the occurrence of spontaneous intermittent pulses of GnRH release, which was observed in control hypothalami of 30- and 50- day-old rats, was reduced to less than 1 pulse/3 h in the presence of buserelin 1 or 10 nM. An hypothalamic action of this GnRH agonist is suggested by these data and should be considered in the evaluation of the therapeutic and possible side effects of buserelin.