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Biomedical subjects

B J Everitt

Publications and source records attributed to B J Everitt.

At least 199 records · Page 11Linked to original sources

Hormonal basis of proceptivity and receptivity in female primates.

The role played by steroid hormones in regulating the sexual behavior of female primates is reviewed, with emphasis placed on experiments using nonhuman species. A distinction is made between the effects of hormones on female proceptivity (i.e., behaviors which incite mounting activity in the male) and receptivity (i.e., willingness to accept male mounting attempts). The rationale for distinguishing between proceptivity and receptivity is discussed, and the methods used for measuring each are described. Evidence shows that estrogen of ovarian origin facilitates sexual interaction primarily by stimulating the emission of non-behavioral cues which increase the female's sexual attractivity (i.e., the value of a female as a sexual stimulant for a male). Evidence is presented suggesting that ostrogen may enhance proceptivity by acting on the female's central nervous system; however, there is no clear demonstration that estrogen affects neural mechanisms controlling receptivity. Experiments show that proceptivity and to a lesser extent receptivity are modulated by adrenal androgens, and the possibility is raised that adrenal androgens may act synergistically with estrogen to facilitate sexual behavior. A disruptive effect of progesterone on sexual interaction is described, and evidence is presented suggesting that this effect of progesterone results primarily from a reduction in sexual attractivity caused by the action of the hormone in the female's vagina. Other literature indicates that proceptivity is often maximal at the periovulatory period of the female primate's menstrual cycle whereas cyclic variations in receptivity occur infrequently. Most hormone-dependent changes in sexual interaction associated with the menstrual cycle seem to result from fluctuations in nonbehavioral attributes of female sexual attractivity. The problem of distinguishing between the effects of steroid hormones on proceptivity and receptivity in human females is discussed.

Androgens↗

Enhancement of sexual behavior in the female rat by nicotine.

The effects of nicotine alone or in combination with mecamylamine, and the effects of both in combination with DA agonists and antagonists and d-LSD (5-HT agonist) have been studied on the sexual behaviour of castrate, estrogen-treated female rats. The results show that nicotine (as low as 50 mug/kg) significantly increases sexual receptivity. The pharmacological analysis suggests this effect to be mediated by a central, nicotine-like cholinergic receptor whose relationship to DA and 5-HT pathways known to exert inhibitory influences on receptivity in the female rat is also discussed.

Animals↗

5-hydroxytryptamine in the central nervous system and sexual receptivity of female rhesus monkeys.

The role of 5-hydroxytryptamine (5-HT) in the control of sexual receptivity in female rhesus monkeys has been studied in 24 adult females paired with 6 adult males. p-Chlorophenylalanine (PCPA, 75 mg/kg or 100 mg/kg, every fourth day), a selective inhibitor of 5-HT, was found to reverse unreceptivity induced by adrenalectomy in ovariectomised, oestrogen-treated females. PCPA-treated females presented more frequently and initiated more sexual behaviour, or else they refused fewer of the male's attempts to mount. These effects were in turn reversed by 5-hydroxytryptophan (5-HTP, 20 mg/kg every second day), when this was given to PCPA-treated animals. In addition, 5-HTP given alone to ovariectomised oestrogen-treated females reduced their receptivity. Parallel biochemical experiments showed that PCPA in the doses used lowered the levels of 5-HT in the brain as measured by the levels of 5-hydroxyindole-3-acetic acid (5-HIAA) in the CSF, and that these were restored by 5-HTP. Both oestradiol benzoate (15 mug/day for 10 days) and testosterone propionate (250 mug/day or 400 mug/day for 10 days) lowered the turn-over rates of 5-HT in the brain (as measured by the probenecid test) in ovariectomised female monkeys. These effects of oestradiol on turnover were antagonised by progesterone (15 mg/day for 10 days, given with oestradiol). A substance other than an adrenal androgen has thus been found to reverse the effects of adrenalectomy on sexual receptivity in female monkeys. It is therefore possible that androgens regulate receptivity in female monkeys by modifying the activity of 5-HT-containing neural systems.

Adrenalectomy↗

The effects of implanting testosterone propionate into the central nervous system on the sexual behaviour of adrenalectomised female rhesus monkeys.

Bilateral adrenalectomy rendered ovariectomised, oestrogen-treated female rhesus monkeys sexually unreceptive. Small unilateral implants of testosterone propionate (mean weight 140 mug) into the anterior hypothalamus/preoptic area restored receptivity in 7 out of 8 of these monkeys. Cholesterol implanted into the same area, or similar amounts of testosterone propionate implanted into the posterior hypothalamus/pretectal area (4 females) or cerebral cortex/dorsal thalamus (5 monkeys) had no consistent effect on behaviour. It therefore seems likely that androgens regulate sexual receptivity in female monkeys by acting on some part of the anterior hypothalamus. Thus, though the hormonal control of receptivity in female primates differs from non-primates, the site on which hormones act to regulate this behaviour may be similar in both.

Adrenal Glands↗

Role of monoamines in the control by hormones of sexual receptivity in the female rat.

The involvement of indole- and catecholamines in the hormonal regulation of sexual receptivity has been investigated in ovariectomized female rats. Drugs that reduce 5-hydroxytryptamine, dopamine, and adrenaline or increase noradrenaline neurotransmission tended to facilitate the occurrence of estrous behavior in estrogen-treated females, and drugs having opposite effects tended to inhibit receptivity induced by estrogen and progesterone. Estrogen decreased noradrenaline turnover in cortex and brain stem; progesterone enhanced this effect in brain stem but prevented it in cortex. Both hormones tended to block noradrenaline uptake in hypothalamus in vitro. In a schedule used to induce receptivity, estrogen accelerated serotonin turnover, an effect prevented by progesterone. Thus a number of monoamines may be involved in the control by hormones of estrous behavior. Furthermore, hormones affect both amine turnover and uptake mechanisms.

Adrenalectomy↗

Action of dopamine receptor agonists in forebrain and hypothalamus: rotational behavior, ovulation, and dopamine turnover.

An ergolene derivative having a piperazine-phenyl side chain instead of a peptide side chain causes rotational behavior in experimental rats and appears to activate mainly limbic DA receptors when given in vivo, in contrast to amino acid ergot alkaloids, which appear to activate all DA receptors when given systemically. Theophyllamine and caffeine were found to cause considerable enhancement of the action of DA formed from DOPAP AND DA receptor agonists such as apomorphine, piribedil, and amino acid alkaloids on supersensitive DA receptors. Many DA receptor agonists such as apomorphine, piribedil, and CB 154 have in common the property to induce hypothermia in mice, an effect that may be related to actions on limbic DA receptors. Many DA receptors agonists such as apomorphine, piribedil, ergocornine, and CB 154 are able to block ovulation in immature rats treated with PMS. It is likely that this blockade is related to activation of a DA receptor in the median eminence controlling LRF secretion. DA receptor agonists antagonize sexual activity in the female rat, whereas DA receptor blocking agents enhance it. DA neurons may therefore subserve an inhibitory role in the control by hormones of sexual behavior. It is of considerable interest that there appear to exist inhibitory DA receptors with regard to both LRF secretion and sexual behavior.

Animals↗