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.     

Facilitation of receptive behavior in estrogen-primed female rats by the anti-progestin, RU 486

The progestin receptor antagonist RU 38486 (henceforth referred to as RU 486) was tested for facilitative effects on female receptive behavior in ovariectomized Long-Evans rats primed with 2 micrograms estradiol benzoate (EB). RU 486 (0, 0.5, 1.6, or 5.0 mg) was administered 48 hr after estrogen priming. The lordosis quotient (LQ) and lordosis score (LS) were assessed 4 hr after RU 486 administration in a standardized test consisting of a 10-mount test by a stimulus male. A significant dose effect was found by both LQ and LS, with those subjects receiving 5 mg of RU 486 being significantly more receptive than vehicle control animals. Thus RU 486 acted as a weak progestin agonist under testing conditions typical for assessment of progestin facilitation of female sexual behavior in rats. Low levels of proceptive behavior (hops and darts) were seen in a minority of the tests, and did not vary systematically as a function of the dose of RU 486 administered. We also examined the effects of RU 486 given before progesterone (P) on receptivity in a blocking paradigm and confirmed previous reports that the antagonist significantly attenuates facilitation of sexual behavior when given in combination with P. A progestin receptor assay of the cytosols of the hypothalamus-preoptic area in estrogen-primed female rats treated with 5 mg RU 486 revealed a significantly greater depletion of available cytosolic P receptors than when rats were treated with a similarly facilitating dose of P (100 micrograms). The results suggest a possible dual mode of action for RU 486--a weak, receptor-mediated agonistic effect on sexual behavior when given alone to estrogen-primed rats, and a competitive blocking effect on receptivity when administered with P.     

Hormonal control of female sexual behavior in the rat

Graded amounts of estradiol benzoate (ranging from 0.48 to 500 μg/kg) were administered to ovariectomized, adrenalectomized female rats in order to analyze the effects of estrogen on the qualitative and quantitative aspects of female reproductive behavior in this species. The interaction of hormone dose and copulatory stimulation was also investigated. In this study, soliciting behavior and lordosis responses were broken down into subcategories. There were three main results. First, it was found that the responses were hierarchically arranged such that, with increasing doses of hormone, the common elements of sexual responding appeared in the same order across individual females. Second, the chronic endocrine background of the female influenced the degree of her receptivity following an acute injection of estrogen. Third, repeated elicitation of lordosis by copulatory stimulation facilitated the subsequent occurrence of lordosis.     

Facilitatory and inhibitory effects of beta-endorphin on lordosis in female rats: relation to time of administration.

The purpose of the present study was to investigate the effect of time of beta-endorphin (beta-EP) administration on lordosis in ovariectomized female rats injected subcutaneously (sc) with estradiol benzoate (EB) and progesterone (Prog). Intracerebroventricular (icv) injections of beta-EP and naloxone (NLX), an opioid receptor antagonist, were administered at the various stages of sc steroid hormone priming. Facilitation of lordosis induced by 10 microg beta-EP was observed exclusively within the initial 6 h of estrogen action, after which inhibition of lordosis occurred. At 12 h after EB priming, at the time of sc Prog treatment (or 43 h after EB priming), icv injection of 10 microg beta-EP significantly inhibited lordosis. Lordosis was significantly facilitated by icv injections of 1 and 10 microg beta-EP at the time of sc EB priming, but not by 0.1 microg beta-EP. A dose-response relationship was identified for lordosis in experimental animals receiving icv injection of beta-EP. Lordosis was inhibited by icv injections of 1 and 10 microg beta-EP at 1 h before the test (or 47 h after EB priming). Lordosis was significantly inhibited by icv injection of NLX at all stages. From the present results, it seems that two different mechanisms are involved in endorphinergic modulation of rats' sexual receptivity: (a) the endorphinergic system at the initial stages of estrogen action facilitates the estrogen activation of lordosis; (b) the endorphinergic system at the final stages of steroid action inhibits lordosis. Moreover, there exists a critical time between 6 and 12 h after estrogen priming for endorphinergic mediation to modulate estrogen action.     

Effects of serotonin agonists on lordosis,myoclonus, and cytoplasmic progestin receptors in guinea pigs

Peripheral treatment with the serotonin releaser fenfluramine or the serotonin agonist quipazine abolished lordosis behavior in ovariectomized estradiol and progesterone-primed female guinea pigs. Quipazine was also effective when administered into a lateral cerebroventricle. The lowest dose of fenfluramine that induced myoclonus (10 mg/kg) was higher than the dose needed to inhibit lordosis (5 mg/kg). Therefore, it appears that myoclonus and lordosis are differentially sensitive to serotonin agonists. The effects of quipazine on lordosis were time dependent. Quipazine had no effect on lordosis when given prior to the onset of sexual receptivity. These data suggest that serotonin agonists might be effective only when progesterone has had sufficient time to induce sexual receptivity. Quipazine did not affect cytoplasmic progestin receptors in brain areas involved in steroid hormone effects on lordosis. This finding, and the finding that quipazine had no effect on lordosis when given prior to the onset of sexual receptivity, suggest increased serotonin transmission does not interfere with estrogen priming or sensitivity of hypothalamic cells to progesterone.     

Facilitation of Sexual Receptivity by Ventromedial Hypothalamic Implants of the Antiprogestin RU 486

RU 486 is known primarily as an antagonist to progestins and glucocorticoids. However, RU 486 has also been shown to have agonistic progestational properties in biochemical and behavioral studies. In the current study, RU 486 was implanted directly into tim ventromedial hypothalamus (VMH) to test for facilitative action on the receptive behavior of female ovariectomized Long-Evans rats primed with 5 μg of estradiol benzoate. Cannulae containing RU 486, progesterone (P), or empty cannulae were implanted 48 hr after estrogen priming. The lordosis quotient and the lordosis score were assessed 4 hr after the cannulae were lowered by a standardized test consisting of 10 mounts by a stimulus male. P and RU 486 significantly facilitated receptivity compared to blank implants in terms of lordosis quotient and lordosis score, with no significant difference between the hormone treatments. While only a single dose of each treatment was given in the current study, RU 486 facilitated lordosis when implanted to the VMH as well as progesterone in contrast to our previous results where the steroids were administered systemically.     

Sauvagine: effects on gastric acid secretion in rats

Intracerebroventricular (ICV) and subcutaneous (SC) injections of sauvagine powerfully inhibited gastric acid secretion stimulated by gastric distension and by 2-deoxy-D-glucose, but not by histamine in pylorus-ligated rats. Naloxone failed to antagonize the antisecretory effects of SC and ICV sauvagine. Intravenous infusion of sauvagine completely suppressed bethanechol-stimulated gastric secretion, significantly decreased pentagastrin-stimulated gastric secretion and did not modify histamine-stimulated gastric secretion in gastric-perfused rats. The inhibitory effect of sauvagine on gastric secretory response is not mediated through opioid or histamine receptors. It appears to be dependent on a vagal mechanism as well as other mechanisms that await further elucidation.     

Effect of various ACTH analogs on lordosis behavior in the female rat

The effect of ACTH and various related analogs on lordosis behavior in female rats was compared with that produced by α-MSH. Ovariectomized rats received 2 μg estradiol benzoate on Day 1 and Day 3 either 0.1 or 0.2 mg progesterone. Four hours later the females were placed with sexually experienced male rats and the lordosis quotient (LQ) noted. These particular doses of progesterone were chosen because they were sub-maximal and produced a proportion of both nonreceptive (LQ less than 50%) and receptive (LQ greater than 50%) rats. Treatment with 20 μg α-MSH on Day 2 stimulated lordosis in nonreceptive rats but inhibited lordosis in the receptive rats.Of the other peptides tested only ACTH4–10 was as effective as α-MSH in facilitating and inhibiting lordosis behavior. ACTH1–24 and ACTH4–9 also produced both effects. ACTH1–39 and ACTH1–16, on the other hand, had neither effect but were both effective in stimulating and inhibiting lordosis when administered on Days 1, 2 and 3. It is suggested that ACTH4–10 may contain the essential sequence for these facilitatory and inhibitory effects on female sexual receptivity and that elongation of the peptide chain beyond ACTH 1–13 (α-MSH) may decrease this activity.     

A tetrapeptide isolated from hamster embryo with central opiate properties on gastrointestinal motility but not on pain perception

The effects of centrally administered kentsin (H-Thr-Pro-Arg-Lys-OH) on intestinal motility and on pain perception were investigated in rats chronically equipped with lateral ventricle catheters. Intestinal motility was recorded electromyographically from electrodes placed on the duodeno-jejunum; analgesia was evaluated by the hot-plate and tail-flick tests. Kentsin (4.0 ug/kg), injected intracerebroventricularly (ICV) 2 hours after the beginning of a meal, restores the "fasted" i.e. the migrating myoelectric complex of intestinal motility, while a 5 times higher dose administered subcutaneously was inactive. The ICV effect of kentsin was blocked by previous ICV administration of naloxone (400 ug/kg). In contrast, kentsin administered ICV (40 ug/kg) or SC (200 ug/kg) did not affect significantly (P greater than 0.05) the time latency in the two analgesic tests during 90 minutes after its administration and did not significantly modify the analgesic effects of (D5-Ala2, Met5) enkephalinamide. We conclude that kentsin when centrally administered acts on opiate receptors to alter gastrointestinal motility but without effects on pain perception.     

Modulation of the arcuate nucleus–medial preoptic nucleus lordosis regulating circuit: A role for GABAB receptors

Estradiol rapidly activates a microcircuit in the arcuate nucleus of the hypothalamus (ARH) that is needed for maximal female sexual receptivity. Membrane estrogen receptor-α complexes with and signals through the metabotropic glutamate receptor-1a stimulating NPY release within the ARH activating proopiomelanocortin (POMC) neurons. These POMC neurons project to the medial preoptic nucleus (MPN) and release β-endorphin. Estradiol treatment induces activation/internalization of MPN μ-opioid receptors (MOR) to inhibit lordosis. Estradiol membrane action modulates ARH gamma-aminobutyric acid receptor-B (GABA_B) activity. We tested the hypothesis that ARH GABA_B receptors mediate estradiol-induced MOR activation and facilitation of sexual receptivity. Double-label immunohistochemistry revealed expression of GABA_B receptors in NPY, ERα and POMC expressing ARH neurons. Approximately 70% of POMC neurons expressed GABA_B receptors. Because estradiol initially activates an inhibitory circuit and maintains activation of this circuit, the effects of blocking GABA_B receptors were evaluated before estradiol benzoate (EB) treatment and after at the time of lordosis testing. Bilateral infusions of the GABA_B receptor antagonist, CGP52432, into the ARH prior to EB treatment of ovariectomized rats prevented estradiol-induced activation/internalization of MPN MOR, and the rats remained unreceptive. However, in EB-treated rats, bilateral CGP52432 infusions 30 min before behavior testing attenuated MOR internalization and facilitated lordosis. These results indicated that GABA_B receptors were located within the lordosis-regulating ARH microcircuit and are necessary for activation and maintenance of the estradiol inhibition of lordosis behavior. Although GABA_B receptors positively influence estradiol signaling, they negatively regulate lordosis behavior since GABA_B activity maintains the estradiol-induced inhibition.     

MSH/ACTH4-10: a tool to differentiate between the role of vasopressin in memory consolidation or retrieval processes

MSH/ACTH4-10 induces a dose dependent increase of latency scores during retention of a passive avoidance response, when injected SC prior to retention but not when administered immediately after the learning trial. Intracerebroventricular administration of anti-vasopressin serum immediately after the learning trial or 1 hr prior to retention induces marked deficits in passive avoidance behavior as indicated by low latencies during retention. SC injection of MSH/ACTH4-10 increased latency scores in animals which received anti-vasopressin serum prior to retention, but did not alter latencies in animals, which received anti-vasopressin serum after the learning trial. These results suggest that MSH/ACTH4-10 is involved in retrieval processes and is able to differentiate between the effects of vasopressin on memory consolidation and on retrieval.     

Proglumide: Selective antagonism of the rumination but not gastric motor effects induced by pentagastrin in sheep

The effect of intravenous (IV) vs intracerebroventricular (ICV) administrations of pentagastrin on gastro-intestinal motility and rumination were investigated by electromyography in sheep ; these effects were compared to those obtained after a previous IV or ICV injection of proglumide. When ICV administered at a dose of 20 ng.kg^?1, pentagastrin did not significantly affect the frequency of reticular and abomasal spiking activity but elicited a 13 to 37 min period of rumination after a delay of 23 ± 7 min. In contrast, when IV infused at a rate of 20 ng.kg^?1.h^?1 during 20 min, pentagastrin inhibited significantly the frequency of reticular and abomasal contractions for 30 to 40 min but did not induce rumination. Proglumide ICV administered (0.8 mg/kg^?1) abolished the rumination induced by central injection of pentagastrin whereas a 10 times higher dose administered systematically (8 mg.kg^?1 IV) did not block these effects. Both of ICV and IV administrations of proglumide at respectively 0.8 and 8 mg.kg^?1 were unable to antagonize the inhibitory effects of pentagastrin on reticulum and abomasum motility.     

Effect of 5 alpha-dihydrotestosterone on sexual receptivity and neural progestin receptors in ovariectomized rats given pulsed estradiol

Experiments were carried out to examine the mechanism whereby 5 alpha-dihydrotestosterone (DHT) antagonizes the stimulatory effects of estrogen plus progesterone (P) on sexual receptivity (lordosis) in the ovariectomized rat. Estradiol (E2; 1 microgram s.c. in 10% ethanol) was administered in a discontinuous (pulsed) treatment regimen thought to mimic phase requirements of estrogen action; two injections of E2 were given either 6 or 12 h apart (first injection, Hour 0). Progesterone (0.5 mg in oil) was injected at Hour 20, and behavioral testing occurred at Hour 24. Dihydrotestosterone (2.5 mg s.c. in 10% ethanol/propylene glycol) inhibited lordosis when it was given before (-12 or -3 h), between (+3, or -3 and +3 h), or after (+8 h) the two E2 injections, but was not effective when given at +20 h. Significant inhibition of E2 + P-induced lordosis was achieved by 2.5 but not 1.0 or 0.2 mg DHT at -3 h, while uterine weights in the same animals were reduced significantly by 2.5 and 1.0 mg DHT. Serum E2 and DHT concentrations peaked rapidly after injection, declining to near baseline by 3 and 12 h, respectively. Induction of cytosolic progestin receptors (cPR) in the preoptic area and medial basal hypothalamus by estrogen was not prevented by DHT when animals were given the two pulsed E2 injections or daily injections of estradiol benzoate, although P was able to override the inhibitory behavioral effects of DHT in the latter but not the former group.(ABSTRACT TRUNCATED AT 250 WORDS)     

Hormonal Modulation of the Cutaneous Initiation of Lordosis in Infant and Adult Rats

The purpose of these experiments is to compare the regional specificity (Experiment 1) and the hormonal modulation (Experiment 2) of the cutaneous initiation of lordosis in 4- to 6-day-old male and female rats (infants) and in 60- to 90-day-old female rats (adults). In Experiment 1, subjects were primed with 100 μg estradiol benzoate (EB) and 0.5 mg progesterone (P) and were denervated on the Waist (dermatomes L1-L3), Midriff (dermatomes T10-L3), Flanks (dermatomes L4-L6), or Sides (dermatomes T10-L6). In infants, there were no significant differences between males and females. Denervation of the Waist. Midriff, or Sides but not of the Flanks significantly decreased the percentage of subjects displaying lordosis, lordosis quotient (LQ), and mean lordosis duration; no significant differences were obtained among Waist-, Midriff-, or Sides-denervated infants. In contrast, denervation of the Sides but not of the Waist significantly decreased LQ and mean lordosis intensity among adults. In Experiment 2, Waist-denervated infants and their surgical Controls were treated either with 100 μg EB and 0.5 mg P or with the oil vehicle; Waist-denervated adults and their surgical Controls received either 100 or 10 μg EB (no P). Regardless of hormone treatment, denervation of the Waist significantly decreased LQ and lordosis duration in infants and decreased LQ and lordosis intensity in adults. In infants, the only effect of priming with EB and P was to increase the percentage of pups showing lordosis and lordosis duration among the surgical Controls. In contrast, priming with 100 μg EB significantly increased the percentage of rats displaying lordosis, LQ, and lordosis intensity among Waist-denervated adults. These data suggest that cutaneous input from the Waist is important for eliciting lordosis in both infant and adult rats, and that the importance of this input is modulated by hormone priming in adult but not infant rats.     

Lordosis behavior in male rats after lesions in different regions of the corticomedial amygdaloid nucleus

The aim of the experiment was to study the effects of stereotaxic lesions of the anterior and the posterior regions of the corticomedial amygdaloid nucleus (CMN) on the display of lordosis behavior by the male rat. Animals were orchidectomized as adults and given estradiol benzoate and progesterone (P) sequentially. Sexual behavior testing was performed by 9 +/- 1 hr after P injection. Lesions placed into the posterior region of the CMN significantly decreased the proportion of animals showing lordosis behavior as compared to sham-operated and control animals. By contrast lesions in the anterior region of the CMN did not cause any changes in the proportion of animals displaying lordosis but markedly increased the lordosis quotient (LQ) of responding animals. The CMN was then concluded to exert a dual control in the display of lordosis behavior in the male rat with a posterior region regulating the willingness of animals to display lordosis behavior and rostral region subserving inhibitory mechanisms related to the sexual performance (LQ values).     

Facilitatory and Inhibitory Effects of β-Endorphin on Lordosis in Female Rats: Relation to Time of Administration

The purpose of the present study was to investigate the effect of time of β-endorphin (β-EP) administration on lordosis in ovariectomized female rats injected subcutaneously (sc) with estradiol benzoate (EB) and progesterone (Prog). Intracerebroventricular (icv) injections of β-EP and naloxone (NLX), an opioid receptor antagonist, were administered at the various stages of sc steroid hormone priming. Facilitation of lordosis induced by 10 μg β-EP was observed exclusively within the initial 6 h of estrogen action, after which inhibition of lordosis occurred. At 12 h after EB priming, at the time of sc Prog treatment (or 43 h after EB priming), icv injection of 10 μg β-EP significantly inhibited lordosis. Lordosis was significantly facilitated by icv injections of 1 and 10 μg β-EP at the time of sc EB priming, but not by 0.1 μg β-EP. A dose–response relationship was identified for lordosis in experimental animals receiving icv injection of β-EP. Lordosis was inhibited by icv injections of 1 and 10 μg β-EP at 1 h before the test (or 47 h after EB priming). Lordosis was significantly inhibited by icv injection of NLX at all stages. From the present results, it seems that two different mechanisms are involved in endorphinergic modulation of rats' sexual receptivity: (a) the endorphinergic system at the initial stages of estrogen action facilitates the estrogen activation of lordosis; (b) the endorphinergic system at the final stages of steroid action inhibits lordosis. Moreover, there exists a critical time between 6 and 12 h after estrogen priming for endorphinergic mediation to modulate estrogen action.     

Can ACTH analogs support discriminative learning in rats?

Ten rats were trained to discriminate between the stimulus properties of subcutaneously (SC) administered MSH/ACTH4-10 and saline in a two-lever, food-motivated operant task. After 12 weeks of discriminative training with 100 micrograms/kg MSH/ACTH4-10, half the rats received 200 micrograms/kg MSH/ATCH4-10, whereas the other half were administered 400 micrograms/kg, for 6 additional weeks. Subsequently, all rats continued training on 50 micrograms/kg ORG 2766 (SC) and, after 12 weeks of training, were randomly assigned to receive either 100 or 200 micrograms/kg ORG 2766. The results of this extensive 36 week training schedule indicate that only 1 of the 10 rats learned to discriminate the interoceptive cues produced by the ACTH analogs. However, this rat's performance was so sustained and errorless that the possibility exists that it was relatively more sensitive to the effects of MSH/ACTH4-10 and its analogs and that these substances may support discriminative learning in the rat.     

Corticotropin-releasing factor receptor subtypes mediating nutritional suppression of estrous behavior in Syrian hamsters

Caloric deprivation inhibits reproduction, including copulatory behaviors, in female mammals. Decreases in metabolic fuel availability are detected in the hindbrain, and this information is relayed to the forebrain circuits controlling estrous behavior by neuropeptide Y (NPY) projections. In the forebrain, the nutritional inhibition of estrous behavior appears to be mediated by corticotropin-releasing factor (CRF) or urocortin-signaling systems. Intracerebroventricular (ICV) infusion of the CRF antagonist, astressin, prevents the suppression of lordosis by food deprivation and by NPY treatment in Syrian hamsters. These experiments sought to determine which CRF receptor type(s) is involved. ICV infusion of the CRF receptor subtype CRFR2-selective agonists urocortin 2 and 3 (UCN2, UCN3) inhibited sexual receptivity in hormone-primed, ovariectomized hamsters. Furthermore, the CRFR2-selective antagonist, astressin 2B, prevented the inhibition of estrous behavior by UCN2 and by NPY, consistent with a role for CRFR2. On the other hand, astressin 2B did not prevent the inhibition of behavior induced by 48-h food deprivation or ICV administration of CRF, a mixed CRFR1 and CRFR2 agonist, suggesting that activation of CRFR1 signaling is sufficient to inhibit sexual receptivity in hamsters. Although administration of CRFR1-selective antagonists (NBI-27914 and CP-154,526) failed to reverse the inhibition of receptivity by CRF treatment, we could not confirm their biological effectiveness in hamsters. The most parsimonious interpretation of these findings is that, although NPY inhibits estrous behavior via downstream CRFR2 signaling, food deprivation may exert its inhibition via both CRFR1 and CRFR2 and that redundant neuropeptide systems may be involved.     

Comparison of the effects of chronic central administration and chronic peripheral administration of islet amyloid polypeptide on food intake and meal pattern in the rat

Islet amyloid polypeptide (IAPP) is postulated to act as a hormonal signal from the pancreas to the brain to inhibit food intake and reduce adipose energy reserves. The present study compared the effects of chronic peripheral and chronic central administration of IAPP on food intake and meal pattern in rats. IAPP was administered subcutaneously (SC) for 7 days at doses of 0, 0.25, 2.5 and 25 pmol kg(-1) min(-1) using an osmotic minipump or administered centrally at doses of 0, 0.025, 0.25 and 2.5 pmol kg(-1) min(-1) using an osmotic minipump connected to an intracerebroventricular (ICV) catheter inserted into the third ventricle. Both SC and ICV infusion decreased total food intake dose-dependently. The minimal effective dose was 2.5 pmol IAPP kg(-1) min(-1) for SC administration and 0.25 pmol kg(-1) min(-1) for ICV infusion. The decrease in food intake produced by infusion of IAPP was mainly due to decreased meal size, although a significant decrease in meal number also occurred at the highest SC and ICV doses. SC administration produced a larger, more persistent decrease in food intake during the light period than in the dark period, while ICV infusion caused a larger, more persistent decrease during the dark period. The 10-fold difference in minimal effective doses indicates that ICV-administered IAPP acted primarily in the brain to inhibit food intake. The difference between the effects of IAPP on meal pattern with the two methods of administration suggests that IAPP does not act on the same target(s) when administered centrally as it does when it is administered peripherally.     

Role of hypothalamic serotonergic receptors in the control of lordosis behavior in the female rat

The role of serotonin in mediating hypothalamic control of sexual behavior in estrone-primed ovariectomized (OVX) rats was studied by comparing the lordotic patterns following medial preoptic (MPOA) and arcuate-ventromedial (ARC-VM) infusions of serotonin (5-HT), methysergide (MS), and vehicle. In the initial experiments, low receptivity (preinfusion receptivity: mean lordosis/mount ratio = 0.164) was maintained by priming each animal with a low dose of estrone 48 hr prior to mating. The infusion of MS in either the MPOA or ARC-VM area resulted in a significant enhancement of lordotic behavior from initial low receptivity, 5-HT infusions were found to have no statistically significant effect upon lordotic behavior. In order to corroborate the findings observed in the low preinfusion receptivity protocol, OVX rats were primed with higher doses of estrone to maintain a high level of receptivity (preinfusion receptivity: mean lordosis/mount ratio = 0.787). Using this protocol, significant depressions in lordotic behavior were observed following MPOA or ARC-VM infusions of 5-HT, It was thus proposed that serotonergic receptors within the MPOA or ARC-VM areas have inhibitory effects upon lordotic behavior. In addition to the effects of 5-HT upon estrogen-induced sexual receptivity, serotonergic influences upon luteinizing hormone-releasing hormone (LRH)-facilitated mating behavior were also evaluated. Comparisons were made between the lordotic responses following MPOA or ARC-VM infusions of vehicle, LRH, or LRH with 5-HT in OVX rats primed with low doses of estrone. The infusion of LRH into the MPOA or ARC-VM significantly enhanced lordotic behavior above vehicle levels. However, the addition of 5-HT to the LRH infusate abolished this behavioral enhancement. These findings indicated that LRH and 5-HT have opposing effects within forebrain areas known to be important for the control of lordotic behavior.