In the present study, the rate constants of degradation (k) and synthesis (S) and half-life of hypothalamic monoamine oxidase were determined to explain annual variations and biphasic effects of the enzyme to low and high doses of estradiol-17 beta (E(2)) in 3-week ovariectomized Heteropneustes fossilis. In the preparatory phase, the half-life (t(1/2)) of the enzyme was the longest (21.16 days) with low k (0.03275 days(-1)) and S (0.000845 Units/day) values, suggesting a low turnover of the enzyme. In the prespawning phase the t(1/2) was the shortest (11.65 days) with high k (0.0595 days(-1)) and S (0.011 Units/day) values. The low and high turnovers of the enzyme, respectively, in these two seasons could be correlated to low and high profiles of plasma E(2) levels. In the resting phase, the values were in between (t(1/2) = 18.83 days, k = 0.0368 days(-1), S = 0.00211 Units/day) but the plasma E(2) level was undetectable. Three weeks of ovariectomy increased the t(1/2) (19.04 days) compared to that of the control (11.61 days) with decreases in both k and S values. The administration of a low dose of E(2) (0.1 mu g/g BW) further increased the t(1/2) (19.04 days) over that of the ovariectomized fish with a significant rise in the S value. However, a high dose of E(2) (1.0 mu g/g BW) decreased it (13.33 days) by reducing the S and elevating the k values. These results suggest that the stimulatory effect of low doses of E(2) on the enzyme activity is produced by elevating its synthesis rate and the inhibitory effect of high doses of E(2) by simultaneously decreasing the synthesis and increasing the degradation rates of the enzyme. The administration of a single dose (75 mg/kg BW) of pargyline has elevated plasma gonadotropin (GTH) level after 3 and 6 hr and 7 days in the sham-ovariectomized (control), ovariectomized, and ovariectomized low-E(2)-dose groups; the peak increase was found at 6 hr. On the contrary, in the ovariectomized high-E(2) group the GTH level was inhibited at 3 and 6 hr postinjection. These changes in the GTH level could be correlated with changes in the profiles of hypothalamic monoamines. The data show that E(2) exerts its feedback regulation of GTH by modifying monoaminergic activity at the level of oxidative deamination. (C) 1995 Academic Press, Inc.