Expression Of Lordosis Behavior Research Articles

Apelin-13 facilitates lordosis behavior following infusions to the ventromedial hypothalamus or preoptic area in ovariectomized, estrogen-primed rats

In normal hormonal conditions, increased neuronal activity in the ventromedial hypothalamus (VMH) induces lordosis whereas activation of the preoptic area (POA) exerts an opposite effect. In the present work, we explored the effect of bilateral infusion of different doses of the apelin-13 (0.37, 0.75, 1.5, and 15 μg) in both brain areas on the expression of lordosis behavior. Lordosis quotient and lordosis reflex score were performed at 30, 120, and 240 min. Weak lordosis was observed following the 0.37 μg dose of apelin-13 at 30 min in the VMH of EB-primed rats; however, the rest of the doses induced significant lordosis relative to the control group. At 120 min, all doses induced lordosis behavior, while at 240 min, the highest dose of 15 μg did not induce significant differences. Interestingly, only the 0.75 μg infusion of apelin in the POA induced significant lordosis at 120 and 240 min. These results indicate that apelin-13 acts preferably in HVM and slightly in POA to initiate lordosis behavior in estrogen-primed rats.

Lordosis facilitation by leptin in ovariectomized, estrogen-primed rats requires simultaneous or sequential activation of several protein kinase pathways

The present study tested the hypothesis that the Janus kinase 2, Src tyrosine kinases, and mitogen-activated protein kinase interact to regulate lordosis behavior induced by leptin in ovariectomized, estrogen-primed rats. The role of protein kinase A and protein kinase C in lordosis facilitation by leptin was also assessed. In experiment 1, the intracerebroventricular administration of leptin to ovariectomized, estradiol-primed rats significantly stimulated lordosis behavior at 1, 2 and 4h post-injection tests. In experiment 2, the Janus kinase 2 inhibitor AG490, the Src tyrosine kinase inhibitor PP2 and the mitogen-activated protein kinase inhibitor PD98059 were administered into the right lateral ventricle before leptin. The lordosis quotient and the lordosis score induced by leptin were significantly decreased by each of these kinase inhibitors. In experiment 3, we examined the effects of RpcAMPS and bisindolylmaleimide, protein kinase A and protein kinase C inhibitors on the lordosis elicited by leptin administration. Lordosis behavior induced by leptin was significantly decreased by both the protein kinase A and protein kinase C inhibitors at 1h post-leptin injection. The results confirm that multiple intracellular pathways participate in the expression of lordosis behavior in estrogen-primed rats elicited by leptin.

Estrogen regulation of noradrenergic signaling in the hypothalamus

Hypothalamic circuits utilizing the monoamine neurotransmitter norepinephrine (NE) may be key elements upon which the ovarian steroids estradiol (E 2) and progesterone (P) act to regulate female reproductive behavior. Recent studies have focused on the modulation of hypothalamic NE release by E 2 and P treatments that facilitate sexual behavior. Brain microdialysis studies suggest that oxytocin, a neuropeptide known to enhance lordosis when infused into the ventromedial hypothalamus (VMH) of E 2 + P-primed females, modulates NE release in the VMH. Systemic administration of oxytocin reliably enhances extracellular NE levels in the VMH of animals primed with moderate doses of both E 2 and P. Thus, ovarian steroids may facilitate female sexual behavior in part by promoting oxytocin-induced NE release in the VMH. Studies examining the release of 3H-NE from superfused hypothalamic slices indicate that estrogen treatment also facilitates NE neurotransmission by attenuating α 2-adrenergic receptor-mediated inhibition of NE release. Hypothalamic α 2-adrenergic receptors are not downregulated by estrogen, suggesting that brain adrenoceptor function can be modulated by E 2 independent of changes in receptor density. A model is proposed wherein E 2 and P enhance hypothalamic NE release, leading to increased excitability of VMH neuronal activity and the expression of lordosis behavior.

Plasma levels of dihydrotestosterone in the cycling rat: Implications for the regulation of lordosis behavior

Exogenously administered dihydrotestosterone (DHT) is a potent inhibitor of sexual behavior in ovariectomized, estrogen-primed rats and endogenous DHT has been implicated as an inhibitor of sexual behavior in cycling rats. To determine the temporal relationship between DHT levels and the expression of sexual behavior, females were tested at midnight of each day of the 4-day estrous cycle for lordosis response to male mounts and subsequently bled. Plasma DHT levels were highest (177±10 pg/ml) at proestrus (P), when lordosis was fully expressed, fell to significantly lower levels (136±8, p<0.025) at estrus (E), and rose at diestrus I and diestrus II (DII) (152±8 and 154±10 respectively). Other female rats were bled from a jugular cannula at 4-hr intervals between midnight of DII and midnight of E. Plasma DHT was elevated from 1200 of P to 0400 of E and fell rapidly through 0800 of E. This elevation of endogenous DHT coincides with the expression of lordosis behavior, and the magnitude of this peak is many times lower than the concentrations reached by the minimal exogenous dose that inhibits lordosis behavior. This suggests that cyclic changes of DHT in the peripheral circulation do not inhibit lordosis behavior during the estrous cycle.

Endogenous progesterone and lordosis behavior in male rats given estrogen alone

Male rats castrated as adults were given successive doses of estradiol benzoate (EB) combined or not with dexamethasone (DEXA) at the end of estrogen treatment. Two experiments were done to determine if progesterone (P) of adrenocortical origin was involved in the display of lordosis behavior under these experimental circumstances. There was a significant rise in blood P concentration in animals given 0.5 and 1.0 μg EB when compared with oil-control injected animals an effect which was completely suppressed by DEXA treatment. An increase in the proportion of estrogen treated animals displaying lordosis responses to male mounts was found with increasing doses of EB and paralleled the effects of EB on P adrenocortical secretion. However the number of feminized animals given 1 μ g EB + DEXA was reduced to the level corresponding to the effects of 0.5 μg EB on lordosis behavior. These data show that the secretion of P by the adrenals is involved in the expression of lordosis behavior in castrated male rats primed with repeated doses of estrogen.

Nonluteal source of lordosis-promoting progesterone secretion in guinea pigs

Prepubertal (21–24 days of age), intact female guinea pigs treated sequentially with estradiol benzoate and LH or FSH displayed lordosis behavior. The gonadotropins apparently caused release of progesterone from the ovaries, because lordosis behavior in guinea pigs is activated by sequential action of estrogen and progesterone. These data demonstrate that immature ovaries, completely devoid of corpus luteum tissue, are capable of secreting behaviorally significant concentrations of progesterone when stimulated by gonadotropins. Therefore, the luteal compartment of the guinea pig ovary is not essential for the preovulatory surges of progesterone that coincide with expression of lordosis behavior in adulthood. Likely candidates for sources of preovulatory progesterone in prepubertal females are antral follicle and interstitial gland tissue.

Ontogeny of biogenic amine systems and modification of indole levels upon adult sexual behavior in the rat

Male, female and androgenized female rats treated on Days 9, 10 and 11 after birth with either 5-HTP or saline were tested for female sexual behavior in adulthood. It was hypothesized that such pharmacological manipulations of the developing serotonergic system in which Day 12 sex differences have been reported might have an influence on the expression of lordosis behavior. No effect of 5-HTP was found in either normal or androgenized females, even though fluormetric analysis indicated a marked increase in endogenous levels of 5-HT at Day 12. However, males treated with 5-HTP has significantly higher 5-HT levels than 5-HT treated control or androgenized females. In addition, fluorometric analysis of norepinephrine, dopamine and serotonin from hypothalamus, mesencephalon and cortex was performed on male and female rats on Days 8, 10, 12 and 14 postnatally to examine the development of various transmitter systems during the early postnatal period.