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R D Lisk

Publications and source records attributed to R D Lisk.

At least 73 records · Page 4Linked to original sources

Prelordotic behavior in the hamster: a hormonally modulated transition from aggression to sexual receptivity.

The behavioral responses of the female golden hamster to a sexually experienced male were analyzed as a function of the stage of the female's estrous cycle. Exogenous estradiol or estradiol followed by progesterone was given to ovariectomized females to determine the role of these hormones in the regulation of cyclic changes in the female's response to the male. Females were paired on a daily basis with sexually active males for 10 min, and behavioral interactions were recorded. Significantly more fighting occurred during early diestrus than later in the cycle. During the 24 hr preceding sexual receptivity, fighting was infrequent. BY 8 HR PRIOR TO THE ONSET OF SEXUAL RECEPTIVITY, 86% OF THE POPULATION EXHIBITED A BEHAVIOR RESEMBLING THE ONSET OF LORDOSIS WITHOUT IMMOBILIZATION (PRELORDOSIS). Following ovariectomy fighting was at a high level (80%--90%). Estradiol replacement, over a 28-day test period, resulted in a significant decrease in aggression and a significant increase in the display of the prelordotic response without inducing lordosis. Initially, the treatment with progesterone following 7 days of estradiol treatment caused the female to display lordosis. After 24 hr a significant increase in aggression, which continued as long as progesterone was present, was observed. After removal of progesterone a significant decrease in aggression occurred. Thus, estradiol causes the female to become tolerant of the male's approach, the female exhibiting prelordosis in response to the male's investigation. Estradiol and progesterone are necessary for normal sexual receptivity; however, after 24 hr, estrogen-progesterone-treated females become agonistic to the male.

Aggression↗

In vivo progesterone treatment enhances [3H]estradiol retention by neural tissue of the female rat.

[3H]Estradiol retention was examined for neural tissues of ovariectomized rats as a function of various progesterone pretreatments. Short-term progesterone pretreatment (6 or 24 h) with a 50 mg pellet of progesteron sc resulted in increased in vivo retention of [3H]estradiol when measured at 6 or 24 h following withdrawal of the progesterone source. This increase was greatest in arcuate-median eminence tissue. A less pronounced increase was seen in the preoptic-anterior hypothalamus and cerebral cortex, and no increase was seen in the amygdala or mammilary bodies. Following long term progesterone pretreatment increased [3H]estradiol retention was observed in vivo at 48, 72, 96 or 120 h in the continued presence of the progesterone source for arcuate-median eminence, preoptic-anterior hypothalamus, amygdala and cerebral cortex. Also, when progesterone pretreatment was 24 h, [3H]estradiol retention was still increased at 36, 48, 60 and 72 h following removal of the progesterone source for arcuate-median eminence, preoptic-anterior hypothalamus, amygdala and cerebral cortex. Our demonstration that progesterone pretreatment can significantly increase [3H]estradiol retention by neural tissue suggests a possible mechanism by which progesterone can regulate the timing of ovulation and sex behavior. Furthermore, our observations are in keeping with the finding that progesterone has little or no effect at the organismal or tissue level unless estrogen is present.

Amygdala↗

Progesterone treatment increases pituitary oestradiol retention in the ovariectomized normal female rat but not in the male nor in the androgen- or oestrogen-sterilized female rat.

Pituitary retention of [3H] oestradiol in ovariectomized rats was measured following in vivo progesterone pre-treatment and found to be significantly increased after 48, 72, 96 and 120 h of pre-treatment. Increased [3H]-oestradiol retention was also observed for at least up to 72 h after removal of the progesterone pre-treatment source. This retention was measured as DPM per mg dry tissue weight. [3H] Oestradiol retention was also measured in the nuclear fraction of tissues incubated with [3H]-oestradiol in vitro. Following 72 h of in vivo progesterone pre-treatment, the nuclear fraction from the pituitary was found to retain significantly more [3H]oestradiol than corresponding fractions from non-treated animals. In contrast to ovariectomized females, no increase in [3H]oestradiol retention was found in the pituitary of orchidectomized males pre-treated with progesterone for 72 h. [3H]Oestradiol retention by pituitaries of ovariectomized rats injected on the day of birth with 200 mug oestradiol benzoate (OeB) or 500 mug testosterone propionate (TP) was significantly decreased in comparison to control animals. When the rats were pre-treated in vivo with oestradiol for 6 or 72 h and [3H]oestradiol retention was measured 6 or 24 h after this pre-treatment, the OeB and TP treated animals retained significantly less [3H]oestradiol under most treatment conditions. Progesterone pre-treatment for 24 or 72 h in vivo followed by measurement of [3H]oestradiol retention immediately or 6 or 24 h later resulted in a significant increase in [3H]oestradiol retention for the control animals. In contrast, the neonatally OeB or TP treated animals differed significantly by not showing increased retention. When [3H]oestradiol retention of the pituitary was measured in vitro following homogenization at 0 degrees C and incubation at 37 degrees C for 1 h, the nuclear fraction from both OeB and TP treated animals was found to retain less hormone per unit DNA; however, this decrease was significant only for the TP animals. Thus, males and androgen- or oestrogen-sterilized females have an altered and reduced augmentation of pituitary oestradiol retention in response to both oestrogen and progesterone pre-treatments.

Animals↗

Dexamethasone: increased weights and decreased [3H] estradiol retention of uterus, vagina and pituitary in the ovariectomized rat.

Ovariectomized rats given 100 mug dexamethasone per day for 5 days had significantly heavier dry weights for uterus, vagina and pituitary, indicating a growth promoting activity of dexamethasone on these tissues in which estrogen normally promotes growth changes. The dexamethasone treated animals also retained significantly less [3H]estradiol per mug dry weight of tissue for uterus, vagina and pituitary. When[3H]estradiol retention was examined in vitro for the nuclear fraction, a significant decrease in retention was found for uterus, vagina and pituitary but not for hypothalamus or cerebral cortex. The decreased ability to bind [3H]estradiol, shown by the estrogen target tissues of the dexamethasone-treated rats, along with the increased growth of the estrogen target tissues, demonstrates that these tissues were able to show trophic responses even when greater levels were one-third of normal. Dexamethasone-treated animals tested for sexual receptivity in the presence or absence of progesterone priming did not show induction of facilitation of sexual receptivity. However, estrogen plus progesterone injections induced sexual receptivity in the presence of dexamethasone. When dexamethasone was combined with a dosage of estrogen, which by itself did not induce sexual receptivity, there was a significant response with 6 to 10 animals showing a low level of receptivity. Thus, dexamethasone can apparently synergize with estrogen to facilitate sexual receptivity.

Animals↗

Progesterone facilitation of sexual receptivity in rats with neural implantation of estrogen.

The neural substrate for estrogen (E) AND E plus progesterone (P)-induced sexual receptivity was examined in 3 classes of adult rats: (1) adult females ovariectomized for 11 days, and (2) females and (3) males gonadectomized on the day of birth. E responses were found only after implantation in the preoptic or medial hypothalamus; adult females had the largest fraction of responders. The addition of P significantly increased the fraction of adult and neonatally ovariectomized females responding when E implantation was made throughout the hypothalamus from preoptic to mammillary bodies. No E-P synergistic effects were seen in the day-1 gonadectomized males. E-P synergistic effects were found in the amygdala of the adult ovariectomized females. However, midbrain implants of E were ineffective for facilitating E-P-induced receptivity in the 3 classes of animals studied.

Animals↗