ESTRADIOL AND ANDROGEN MODULATE CHICKEN LUTEINIZING-HORMONE-RELEASINGHORMONE-I RELEASE IN-VITRO

Hypothalamic slices (1 mm) including medial basal hypothalamus and pre optic areas (MBH-POA) were taken from adult male Japanese quail placed in a short-term perifusion system, and exposed to estradiol or androg en Release of chicken LHRH I (cLHRH-I) was measured by an enzyme immun oassay specific for cLHRH-I. In separate experiments, MBH-POA slices w ere exposed shortterm to 5 alpha-dihydrotestosterone (5 alpha-DHT, 10( -7) M) and testosterone (T, 10(-7) M), and short- or long-term to 17 b eta estradiol (E(2), 10(-9) M). Release of both basal and stimulated c LHRH-I (15-min exposure to 10(-6) M norepinephrine [NEI]) was monitore d. Basal cLHRH-I release during perifusion 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 13.38 +/- 0.5 9 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 +/- 3.03 pg/5 min. Short-t erm E(2) exposure significantly (P < 0.01) potentiated NE-induced cLHR H-I release. Neither T nor 5 alpha-DHT affected baseline or NE-stimula ted cLHRH-I release. Pretreatment with E(2) (10(-9) M) for 14 h in sta tic culture before perifusion significantly (p < 0.05) reduced the NE- induced cLHRH-I release. These results suggest that a hypothalamic LHR H-I pulse-generating mechanism is located within the MBH-POA. Further, these data provide evidence for E(2) modulation of cLHRH-I release, w hich varies with exposure.