Hypothalamic slices (1 mm) including medial basal hypothalamus and preoptic areas (MBH-POA) were taken from adult male Japanese quail, placed in a short-term perifusion system, and exposed to estradiol or androgen. Release of chicken LHRH-I (cLHRH-I) was measured by an enzyme immunoassay specific for cLHRH-I. In separate experiments, MBH-POA slices were exposed short-term to 5 alpha-dihydrotestosterone (5 alpha-DHT, 10(-7) M) and testosterone (T, 10(-7) M), and short- or long-term to 17 beta estradiol (E2, 10(-9) M). Release of both basal and stimulated cLHRH-I (15-min exposure to 10(-6) M norepinephrine [NE]) was monitored. Basal cLHRH-I release during perfusion was episodic throughout the experimental periods. During no treatment, there was a mean (+/- SEM) pulse interval of 21.27 +/- 1.03 min, pulse duration of 13.98 +/- 0.59 min, pulse duration of 13.98 +/- 0.59 min, pulse amplitude of 4.12 +/- 0.13 pg/5 min, and pulse frequency of 2.93 +/- 0.12/h. Mean cLHRH-I pulse amplitude significantly (p < 0.05) increased with challenge by NE to 25.03 +/- 3.09 pg/5 min. Short-term E2 exposure significantly (p < 0.01) potentiated NE-induced cLHRH-I release. Neither T nor 5 alpha-DHT affected baseline or NE-stimulated cLHRH-1 release. Pretreatment with E2 (10(-9) M) for 14 h in static culture before perifusion significantly (p < 0.05) reduced the NE-induced cLHRH-I release. These results suggest that a hypothalamic LHRH-I pulse-generating mechanism is located within the MBH-POA. Further, these data provide evidence for E2 modulation of cLHRH-I release, which varies with exposure.