Interactions between estrogen and progesterone in neural tissues that mediate sexual behavior of guinea pigs

(1) Interactions of estrogen and progesterone with each other and with the neural tissues that regulate sexual behavior in female guinea pigs were studied. (2) Long-acting preparations of estradiol-17β (E 2) were more effective in facilitation of lordosis than other estrogens. (3) A major behavior-f...

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Veröffentlicht in:Psychoneuroendocrinology 1977-01, Vol.2 (4), p.337-347
Hauptverfasser: Feder, H.H., Landau, I.T., Marrone, B.L., Walker, W.A.
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Sprache:eng
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Zusammenfassung:(1) Interactions of estrogen and progesterone with each other and with the neural tissues that regulate sexual behavior in female guinea pigs were studied. (2) Long-acting preparations of estradiol-17β (E 2) were more effective in facilitation of lordosis than other estrogens. (3) A major behavior-facilitating site of action of E 2 is in the medial basal hypothalamus. (4) E 2 is selectively taken up by a saturable receptor system in fractions of hypothalamic tissue. (5) Although early effects of E 2 on neural tissues that mediate lordosis can be mimicked by certain anti-estrogens, anti-estrogens do not mimic long-term effects of E 2 that are required for optimum expression of lordosis behavior. (6) Progesterone (P) is required in extremely small quantities for facilitation of lordosis behavior in estrogen-primed female guinea pigs. (7) Facilitation of sexual behavior is a short-term effect of P that is mediated by the medial basal hypothalamus. (8) P inhibits the expression of lordosis behavior via a mechanism that is represented in the midbrain. (9) This inhibitory action of P has a longer latency than the facilitatory action of P. (10) Prolonged residence of E 2 in the hypothalamus temporarily favors the expression of short-term facilitatory actions of P on lordosis. (11) The long-term lordosis-antagonizing effects of P are not due to inhibition of E 2 uptake in the hypothalamus. (12) Inhibitory effects of P on lordosis may not depend on neural cells that have the ability to concentrate E 2 in their nuclei.
ISSN:0306-4530
1873-3360
DOI:10.1016/0306-4530(77)90003-8