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At least 253 records · Page 14Linked to original sources
PubMed1993

Nerve growth factor affects defense-related behaviors, but not lordosis, in ovariectomized, estrogen-treated rats.

Effects of NGF and anti-NGF on estrogen-sensitive behaviors were examined in ovariectomized, estrogen-treated rats. Intracerebroventricular (i.c.v.) administration of NGF resulted in a significant decrease in body weight. Daily treatment with low levels of estradiol resulted in a steady increase in lordosis behavior as reflected by average lordosis quotient and lordosis score. No effects of NGF or anti-NGF on lordosis behavior were detected. Estrogen treatment also resulted in a significant increase in the number of vocalizations elicited from female controls by male contact during sex behavior. NGF-treatment enhanced this effect, resulting in significantly more vocalizations elicited earlier in the course of estrogen treatment than were elicited from non-NGF-treated controls. These effects were blocked by progesterone. An increase in the number of rejections elicited by male contact during sex behavior was also observed in NGF-treated animals relative to controls. In addition, i.c.v. infusions of anti-NGF prevented the estrogen-mediated increase in elicited vocalizations, suggesting that NGF may have a physiological role in regulating this behavior. These data implicate NGF in the regulation of specific defense-related behaviors in estrogen-treated rats. Effects of NGF and anti-NGF on immunocytochemical staining for p75NGFR-, and ChAT-like immunoreactivity were also analyzed and are discussed.

Aggression↗
PubMed1995

In vitro electro-pharmacological and autoradiographic analyses of muscarinic receptor subtypes in rat hypothalamic ventromedial nucleus: implications for cholinergic regulation of lordosis.

Muscarinic agonists can act through the hypothalamic ventromedial nucleus (VMN) to facilitate lordosis. To elucidate the neuronal mechanism(s) underlying this muscarinic facilitation, effects of muscarinic agents on the single-unit activity of VMN neurons recorded in brain tissue slices of estrogen-primed female rats were analyzed. All the agonists tested, including acetylcholine (ACh), oxotremorine-M (OM), carbachol (CCh) and McN-A-343 (McN), evoked primarily excitation (80-100%), some inhibition (0-20%) and occasional biphasic responses (0-8%). By comparing the response magnitude and the effectiveness in evoking a response, the rank order for evoking excitation, the primary response, was found to be: OM > CCh > ACh approximately McN, which is consistent with that (OM > CCh > McN) for facilitating lordosis reported by others. This consistency and the frequency of its occurrence suggest that the excitatory electric action of the muscarinic agonists is related to their facilitatory behavioral effect. Experiments with antagonists selective for M1 (pirenzepine), M2 (AF-DX 116) and M3 (4-DAMP and p-F-HHSiD) indicate that muscarinic excitations are mediated by M1 and/or M3, but not M2. Since M1 receptors have been shown to be neither sufficient nor necessary to mediate the muscarinic facilitation, M3 receptor may be crucially involved in this behavioral effect. Autoradiographic assays of binding to [3H]4-DAMP with or without pirenzepine and AF-DX 116, also indicate the presence of M3 receptors in the VMN. Quantitative analyses show that the M3 binding was not affected by the in vivo estrogen priming required to permit muscarinic agonists to facilitate lordosis. Thus, while the excitation mediated by M3 is likely to be involved in muscarinic facilitation of lordosis, the regulation of M3 receptor density does not seem to be involved in the permissive

Animals↗
PubMed1986

Effects of 5-HT1A selective anxiolytics on lordosis behavior: interactions with progesterone.

Ipsapirone and gepirone, but not buspirone, facilitated lordosis in estrogen-treated rats, whereas all three drugs inhibited this behavior in rats treated with estrogen and progesterone. When administered at higher doses, ipsapirone, gepirone and buspirone inhibited lordosis in rats treated with either estrogen or estrogen and progesterone. These data are consistent with the proposal that 5-HT1A receptors mediate lordosis-inhibiting effects of 5-HT, and further suggest that some 5-HT1A agonists may facilitate lordosis by activity at autoreceptors. Finally, these data show that progesterone may modulate activity at 5-HT1A receptors.

8-Hydroxy-2-(di-n-propylamino)tetralin↗
PubMed1984

Impaired lordosis response in golden hamsters with lesions in the ventromedial midbrain.

Lesions in the ventromedial midbrain tegmentum of female golden hamsters produced various degrees of impairment of the lordosis response to male hamsters or manually delivered somatic stimuli. The most severe deficits were produced by anterior lesions, whereas larger, more posterior lesions sometimes produced no lordosis impairment. In tests where lordosis was not completely eliminated, the lesions tended to impair maintenance rather than elicitation of lordosis, thus constituting a different behavioral effect from that associated with deep tectal or central gray lesions in this species.

Animals↗
PubMed1989

GABAergic drugs and lordosis behavior in the female rat.

Agents modifying GABAergic neurotransmission were administered to ovariectomized rats treated with different doses of estradiol benzoate (EB) + progesterone (P) or with EB alone. Hormone treatments were designed to induce an intermediate level of receptivity in order to be able to observe both stimulatory and inhibitory effects on lordosis behavior. Both the GABAA receptor agonist THIP and the GABAB receptor agonist baclofen inhibited lordosis behavior at doses from 20 and 5 mg/kg, respectively. The GABA transaminase inhibitor gamma-acetylen GABA (GAG) and the GABA agonist 3-aminopropanesulfonic acid had no effects, even when high doses were administered. The GABAA receptor antagonist bicuculline had no effect by itself nor did it block the effects of THIP. It is therefore suggested that the GABAA receptor is of slight importance in the control of lordosis behavior. No evidence could be found supporting the hypothesis that an interaction between P and GABA is important for hormone-induced receptivity. It does not appear likely that motor disturbances are responsible for the inhibitory effects of baclofen and THIP. The exact mechanism by which these drugs inhibit lordosis behavior is not clear at present.

Alkynes↗
PubMed1986

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 microgram 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 microgram EB + DEXA was reduced to the level corresponding to the effects of 0.5 microgram 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.

Animals↗
PubMed1986

Methysergide inhibits and facilitates lordosis behavior in the female rat in a time-dependent manner.

Reports in the literature have indicated a facilitatory effect of the serotonin antagonist methysergide on lordosis behavior, suggesting an inhibitory role for serotonergic activity. In the present series of experiments, methysergide (7 mg/kg) was found to inhibit lordosis behavior 30 min after intraperitoneal administration to females, treated chronically with estradiol benzoate, or acutely with estradiol benzoate and progesterone. However, methysergide was found to facilitate lordosis behavior 200 and 300 min after administration to female rats treated acutely with estradiol benzoate. These data suggest a time-dependent inhibitory effect of methysergide, and are consistent with the hypothesis that the activity of serotonin type 2 receptors facilitates lordosis behavior in the female rat.

Animals↗
PubMed1986

Facilitation of lordosis behavior in ovariectomized estrogen-primed rats by medial preoptic implantation of 5 beta, 3 beta, pregnanolone: a ring A reduced progesterone metabolite.

The effect on lordosis behavior of progesterone (P) and some of its ring A reduced metabolites (5 beta pregnane 3 alpha ol 20 one, 5 beta pregnane 3 beta ol 20 one and 5 alpha pregnanes 3 beta ol 20 one) was studied in estrogen primed overiectomized rats by unilaterally implanting them in two brain areas related to the control of lordosis behavior: the ventromedial hypothalamic nucleus (VMH) and the medial preoptic area (mPOA). Of the four pregnanes studied only 5 beta 3 beta pregnanolone consistently induced lordosis behavior when implanted into the mPOA. The present results show that some 5 beta reduced P metabolites can facilitate with a short latency the display of lordosis behavior, probably by depressing the activity of telencephalic neurons inhibitory to sexual behavior.

Animals↗
PubMed1988

Injections of cholecystokinin into the ventromedial hypothalamic nucleus inhibit lordosis behavior in the rat.

In the central nervous system, the ventromedial nucleus of the hypothalamus (VMH) is a primary locus for the induction of lordosis behavior by estrogen. Tissue levels of cholecystokinin and its binding sites in the VMH are modulated by estrogen, suggesting a role for cholecystokinin in the regulation of lordosis behavior. The effects of exogenous cholecystokinin octapeptide (CCK-8) were examined by injecting CCK-8 into the VMH and measuring the frequency of lordotic responses. CCK-8 inhibited the frequency of lordotic responses in a dose-related fashion when the control rats had lordosis quotients of 60 and above. This inhibition is in agreement with previously reported results after peripheral injection of CCK-8, and is consistent with the hypothesis that CCK-8 in the VMH in involved in the regulation of lordosis behavior in the estrogen-primed rat.

Animals↗
PubMed1989

Microinjection of cholecystokinin into the medial preoptic nucleus facilitates lordosis behavior in the female rat.

We examined the effect of cholecystokinin (CCK) on lordosis behavior when administered into the medial preoptic area or the nucleus accumbens (NAcc) of ovariectomized estrogen-primed female rats. The frequency of lordotic responses was measured subsequent to unilateral microinjections of sulphated octapeptide CCK (sCCK-8) into the medial preoptic nucleus (MPN) or the NAcc. In the first experiment, three doses of sCCK-8 (1, 5, and 50 ng) microinjected into the MPN, and 50 ng injected into the NAcc produced a marked facilitation of lordosis. In a separate experiment, unilateral injections of an undiluted sCCK-8 antiserum into the MPN produced significant reduction in lordosis behavior in highly receptive females when compared with a normal rabbit serum injected control group. The results of the present study indicate that the CCK innervation of the MPN is involved in the neural regulation of lordosis behavior in the female rat.

Animals↗
PubMed1989

Scopolamine inhibition of lordosis in naturally cycling female rats.

Cholinergic antagonists, such as scopolamine, atropine, and hemicholinium-3, have been found previously to inhibit lordosis in ovariectomized rats primed with estrogen and progesterone. The present study further examined this effect using intact cycling female rats. Cycling was determined by daily monitoring of sexual behavior and vaginal cytology. In the first experiment, intraventricular administration of the muscarinic receptor blocker, scopolamine, was found to significantly inhibit lordosis behavior during natural estrus (10 or 20 micrograms bilaterally). In the second experiment, systemic administration of scopolamine was also found to significantly inhibit lordosis behavior during natural estrus (4 mg/kg, IP). Administration of the cholinergic antagonist did not significantly interrupt cyclicity patterns. These results indicate that central cholinergic muscarinic systems contribute to the regulation of lordosis during natural behavioral estrus in intact female rats.

Animals↗
PubMed1993

Suppression of the lordosis reflex of female rats by efferents of the medial preoptic area.

In freely moving, estrogen- and progesterone-treated ovariectomized female rats, electrical stimulation of the medial preoptic area, which had been isolated dorsally from the septum by a horizontal knife cut (roof cut), caused immediate interruption of the lordosis reflex, a principal component of female reproductive behavior in this species. Neither the knife cut nor the stimulation affected their proceptive interactions with the males. Lordosis was interrupted in a graded manner in response to increased stimulus intensity, with a threshold at 30 microA. The optimal frequency was at 50-100 Hz. Lordosis was reinstated promptly by the termination of current application. The rapid time course distinguished the stimulation effect in the rats with the roof cut from that in the intact control animals, which was slow in its onset and recovery. In the sham-operated animals, an adjunct bilateral cut of the stria terminalis was sufficient to restore the rapid response as in the roof-cut animals. The roof-cut animals were sensitive to lower doses of estrogen than those without the knife cut; therefore, the preoptic area appears to be a separate entity from the septum in the inhibitory control of lordosis. The elimination of facilitatory neural components for this reflex, which enter the preoptic area dorsally via the stria terminalis, might be responsible for the prompt and exaggerated stimulation effect in the roof-cut animals.

Afferent Pathways↗
PubMed1995

Inhibition of lordosis in female hamsters and rats by 8-OH-DPAT treatment.

In the present experiments, the ability of the 5-HT1A agonist, 8-OH-DPAT, to inhibit lordosis was determined in ovariectomized hamsters and rats under various hormonal conditions. Systemic administration of 8-OH-DPAT (0.25 mg/kg) significantly inhibited lordosis duration in ovariectomized hamsters treated on 3 consecutive wk with estradiol benzoate (3 or 10 micrograms) and progesterone (500 micrograms). Similarly, systemic administration of 8-OH-DPAT (0.25 mg/kg) significantly inhibited lordosis frequency in ovariectomized rats treated on 3 consecutive wk with estradiol benzoate (0.25, 0.5, or 25 micrograms for 3 days) and progesterone (500 micrograms), although females treated with the higher doses of estrogen were slightly less inhibited on the second and third wk of testing. Results indicate that the 5-HT1A agonist, 8-OH-DPAT, effectively inhibited lordosis in female hamsters, as well as female rats, under varied hormonal conditions.

8-Hydroxy-2-(di-n-propylamino)tetralin↗
PubMed1994

Two types of lordosis-inhibiting systems in male rats: dorsal raphe nucleus lesions and septal cuts.

To examine the functional relationships between the dorsal raphe nucleus and the septum in the inhibitory regulation of feminine sexual behavior in male rats, castrated male rats received destruction of the dorsal raphe nucleus (DRL), interruption of the septal outputs (ARD), or both DRL and ARD (DRL+ARD). All animals were treated with estradiol by using Silastic tubes, and feminine sexual behavior was observed every other day for 10 days. Most castrated control male rats did not show lordosis throughout the tests. In contrast, all of the males with DRL alone or ARD alone displayed lordosis, but the lordosis quotients (LQ) in these groups were lower than those of the female control group. On the other hand, DRL+ARD males showed higher LQs than the DRL or the ARD males, being comparable to control females. Thus, two types of strong inhibitory influence exist in the dorsal raphe nucleus and the septum, and resist the facilitation of feminine sexual behavior by estrogen in male rats. Furthermore, these inhibitory systems operate independently, because an additive effect of DRL and ARD in facilitating lordosis was clearly observed in DRL+ARD males.

Animals↗
PubMed1994

Effects of hormonal treatment and history on scopolamine inhibition of lordosis.

The muscarinic receptor blocker, scopolamine, inhibits the display of lordosis behavior in female rats but its effectiveness depends on hormonal conditions. In these experiments, systemic administration of scopolamine (0.031-4 mg/kg) inhibited lordosis in ovariectomized rats brought into receptivity by treatment with a low dose of estradiol benzoate (EB, 0.25 micrograms for 3 days) with progesterone (P, 500 micrograms for 1 day), or a high dose of EB (25 micrograms for 3 days) with and without P. However, the effectiveness of scopolamine was reduced at the high dose of EB and with the addition of P. Furthermore, scopolamine failed to inhibit lordosis in females treated on a second week with the high dose of EB with or without P, unless an interval of at least 3 weeks separated the two sets of steroid treatments. The reduced effectiveness of scopolamine cannot be explained by peripheral mechanisms because its inhibitory effect on lordosis also was reduced following repeated hormonal exposure even when scopolamine was infused directly into the lateral ventricles.

Acetylcholine↗
PubMed1995

Interaction between glutamate and luteinizing hormone-releasing hormone (LHRH) in lordosis behavior and luteinizing hormone release (LH): further studies on NMDA receptor mediation.

The present studies examine the effects of the glutamate agonist N-Methyl-D-Aspartic acid on lordosis responsiveness and LH release in estrogen-primed, ovariectomized rats. Groups of rats previously cannulated in the 3rd ventricle of the brain (IVT) were challenged with saline, NMDA and LHRH. A clear increase in lordosis-to-mount quotients (LQ) after IVT administration of 0.5, 0.75 and 1 microgram NMDA was found. LHRH (150 ng IVT) also enhanced LQ. High plasma LH levels were present in both cases. Intraventricular administration of the selective LHRH antagonist [D-p-Glu1, D-Phe2, D-Trp3,6]-LHRH (100 ng) was unable to prevent NMDA action on lordosis behavior. In contrast, it blunted LHRH enhancement of LQ. LH release evoked by either NMDA and LHRH was blocked by the LHRH antagonist. Present results support our previous view suggesting that glutamate, through NMDA receptors, participates in the regulation of lordosis behavior. Glutamate seems to exert its actions in the behavioral and endocrine patterns through different mechanisms; the first seems not to be mediated by LHRH, but the endocrine effect operates via LHRH release.

Animals↗
PubMed1993

Pargyline-induced increase in serotonin levels: correlation with inhibition of lordosis in rats.

The effect of intrahypothalamic infusion of the monoamine oxidase inhibitor pargyline on lordosis behavior and monamine levels in the preoptic area and hypothalamus was examined. Progesterone-facilitated lordosis was blocked by pargyline in half the treated rats. The inhibition of lordosis was correlated with increases in serotonin and dopamine levels in the ventromedial nucleus of the hypothalamus and serotonin levels in the arcuate nucleus-median eminence when compared to controls or pargyline-treated rats with high levels of lordosis responding. Changes in norepinephrine levels were not correlated with changes in behavior. The results provide further evidence for an inhibitory role of basomedial hypothalamic serotonin in the control of female sexual behavior.

Animals↗
PubMed1994

Hypothalamic infusion of the 5-HT2/1C agonist, DOI, prevents the inhibitory actions of the 5-HT1A agonist, 8-OH-DPAT, on lordosis behavior.

Sexually receptive, intact, proestrous rats were infused bilaterally into the ventromedial nucleus of the hypothalamus (VMN) with 200 ng of the 5-HT1A agonist, 8-hydroxy-2-(di-n-propylamino)tetralin (8-OH-DPAT), with 2000 ng of the 5-HT2/1C agonist, (+/-)-(2,5-dimethoxy-4-iodophenyl)-2-aminopropane HCl (DOI), or with both 8-OH-DPAT and DOI. Alone, VMN infusions of 8-OH-DPAT, but not DOI, inhibited lordosis behavior. When 2000 ng DOI was infused simultaneously with 8-OH-DPAT, the inhibitory effects of 8-OH-DPAT were completely abolished. These results suggest that neural sites responsible for the reported facilitatory effects of 5-HT2/1C agonists on lordosis behavior coexist in the VMN with those sites in which 5-HT1A agonists are effective in reducing lordosis behavior. In contrast to the protective action of the 5-HT2/1C receptor agonist following VMN infusion, no protection was seen when both DOI and 8-OH-DPAT were administered intraperitoneally. Thus, the interaction of these two receptor subtypes in the control of lordosis behavior may be different in regions outside the VMN.

8-Hydroxy-2-(di-n-propylamino)tetralin↗