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At least 199 records · Page 11Linked to original sources
PubMed1996

5-HT1A receptor antagonists and lordosis behavior.

In proestrous rats, serotonin 1A (5-HT1A) receptor agonists inhibit lordosis behavior within 5-15 min following infusion into the ventromedial nucleus of the hypothalamus (VMN). In the present report, the lordosis-inhibiting effects of the 5-HT1A agonist [(+/-) 8-hydroxy-2- (di-n-propylamino) tetralin) (8-OH-DPAT] were shown to be attenuated with 5-HT1A receptor antagonists. Two compounds, propranolol and pindolol, that function as both beta-adrenergic and 5-HT1A receptor antagonists, and (+) WAY100135 (chiral N-t-butyl-3-(1-(4-(2-methoxy) phenyl)piperazinyl)-1-phenylpropionamide dihydrochloride, quarter hydrate), a more selective 5-HT1A receptor antagonist, were found to reduce the lordosis-inhibiting effects of 8-OH-DPAT infusion into the VMN. Proestrous rats were co-infused into the VMN with 200 ng 8-OH-DPAT plus 1000 ng or 2000 ng pindolol, 1000 ng or 2000 ng propranolol, or 2000 ng (+) WAY100135. Co-infusion with 1000 ng or 2000 ng pindolol attenuated the inhibitory effects of 8-OH-DPAT; co-infusion of 1000 ng, but not 2000 ng, propranolol, reduced the effects of 8-OH-DPAT; and co-infusion with 2000 ng (+) WAY100135 attenuated the effects of 8-OH-DPAT. Bilateral VMN infusion with 2500 ng (+) WAY100135 facilitated lordosis behavior in suboptimally, hormone-primed ovariectomized rats. These findings strengthen the argument that the inhibitory effect of 5-HT1A receptor agonists on lordosis behavior is the result of their activation of VMN 5-HT1A receptors.

8-Hydroxy-2-(di-n-propylamino)tetralin↗
PubMed1983

Forebrain and lower brainstem participation in facilitatory and inhibitory regulation of the display of lordosis in female rats.

Neural transection of the dorsal extrahypothalamic descending afferents by means of an L-shaped Halász knife at the anterior commissure (anterior roof deafferentation. ARD) markedly potentiated the display of lordosis and soliciting behaviors. Bilateral lesions of the ventromedial hypothalamus (VMH) attenuated lordotic activity in the ARD sham females but not in the ARD females. In contrast, the lesions in the pontine central gray concurrently with ARD effectively inhibited the display of lordosis but not soliciting behaviors. These results suggest that the VMH may not be a primary focus of the dorsal extrahypothalamic inhibitory influence on lordosis. The influence of this inhibitory system seems to be dominant in regulating the expression of lordosis behavior, compared to that of the hypothalamic lordosis facilitating system. Furthermore, the dorsal extrahypothalamic inhibitors influence which could be removed by ARD must be modified by the neural mechanism in the lower brain stem in which the pontine central gray may be actively involved.

Animals↗
PubMed1985

The effects of unilateral frontolateral hypothalamic knife cuts and asymmetrical unilateral septal lesions on lordosis behavior of rats.

It has been shown that the medial hypothalamus exerts facilitatory control over female sexual behavior in the rat whereas the septal area exerts inhibitory control over lordosis behavior. The present study assessed whether the septal area exerts its inhibitory control over lordosis behavior via efferent connections with the mediobasal hypothalamus. Anatomical studies using retrograde tracers verified that cell bodies located in the lateral septal area project ipsilaterally to the mediobasal hypothalamus. Based upon the predominantly ipsilateral connection between the lateral septum and mediobasal hypothalamus, unilateral frontolateral knife cuts were produced on the left or right side of the mediobasal hypothalamus or else sham surgeries. Subsequently all animals were given unilateral electrolytic septal lesions on the right side of the brain. These animals had septal damage that was located either ipsilateral or contralateral with respect to the knife cuts. Female sexual behavior was tested following the hypothalamic knife cuts and retested after unilateral septal lesions. Unilateral hypothalamic knife cuts on either side of the brain had no detectable effect on female sexual behavior when compared to the sham group. However, following unilateral septal lesions a significant increase in lordosis behavior was observed in all groups following treatment with estrogen alone. There were no differences in lordosis behavior between the groups which had septal lesions located ipsilateral vs. contralateral with respect to the hypothalamic knife cuts. These results support the hypothesis that the facilitation in lordosis behavior associated with electrolytic septal lesions is not mediated by neural connections between the septal area and mediobasal hypothalamus. These two brain areas thus appear to exert separate and independent control over female sexual behavior.

Animals↗
PubMed1988

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 less than 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.

Animals↗
PubMed1989

Intrahypothalamic injection of RU486 antagonizes the lordosis induced by ring A-reduced progestins.

We explored the possibility that ring A-reduced progestins facilitate lordosis in estrogen primed rats through their interaction with an intracellular progestin receptor (PR) by using RU486. This drug binds with high affinity to the PR, thus preventing the action of progesterone (P). Ovariectomized estrogen-primed rats (2 micrograms estradiol benzoate 40 hr earlier) were bilaterally injected into the ventromedial hypothalamic nucleus (VMHN) with 1 microgram of: P, 5 alpha-pregnanedione or 3 beta,5 beta-pregnanolone in 1 microliter oil. All three progestins effectively facilitated lordosis, tested at four and eight hours after intrahypothalamic injections. The ability of RU486 to counteract progestin-induced lordosis was assessed by infusing 10 micrograms of this agent into the VMHN along with any of the progestins. RU486 antagonized the lordosis induced not only by P (67% reduction) but also that induced by 5 alpha-pregnanedione and by 3 beta,5 beta-pregnanolone (47% and 93% reductions, respectively). Results suggest that ring A-reduced progestins may act through the PR mechanism to facilitate lordosis, i.e., in a fashion similar to P.

5-alpha-Dihydroprogesterone↗
PubMed1991

Role of the ventromedial nucleus of hypothalamus in the male-induced enhancement of lordosis in female rats.

The involvement of the ventromedial nucleus of the hypothalamus (VMH) in the mating-induced enhancement of lordosis in ovariectomized estrogen-primed rats was investigated. In the first experiment, females with bilateral VMH or sham lesions were primed with 2 micrograms estradiol benzoate, and 48 h later they were subjected to repeated-mating tests. The VMH-lesioned rats failed to exhibit lordosis during the tests; however, the sham-operated females exhibited a gradual increase in lordosis quotient (LQ) with repetitive matings. In the second experiment, ovariectomized females were bilaterally implanted with estradiol (E2) or cholesterol (C) in the VMH, 48 h prior to behavioral testing. Repeated-mating-induced elevation in LQ was observed in the females when they were bilaterally implanted with E2 in the VMH; C was ineffective. To exclude the possibility of the spread of E2 to areas adjacent to VMH, plasma-luteinizing hormone (LH) was measured. Elevation in the circulating LH levels following ovariectomy was not suppressed in the females following bilateral E2 implants in the VMH, suggesting that the effect of estrogen is localized within or immediately around the VMH. The results suggest that the integrity of the VMH is critical for the potentiation of lordosis behavior in ovariectomized estrogen-primed females by male-originating sensory cues, and that selective priming of the VMH with estrogen is sufficient for the male-induced enhancement of lordosis.

Animals↗
PubMed1992

Lordosis in male rats: the facilitatory effect of mesencephalic dorsal raphe nucleus lesion.

The dorsal raphe nucleus was destroyed (DRL) by a radiofrequency lesion generator in castrated male rats, and lordosis behavior was observed. Five weeks after the surgery, all animals were implanted with two Silastic tubes containing estradiol (E2). Behavioral tests were started 2 days after implantation of E2 and carried out every other day for 16 days. Castrated control and sham-operated control males showed low incidence of lordosis and low lordosis quotient (LQ) throughout the tests, whereas all the DRL males displayed lordosis and the mean LQ of the group was significantly higher than that of control groups, but lower than that of an ovariectomized female group. These results suggested that the dorsal raphe nucleus plays an important role in inhibiting lordosis in male rat brain.

Animals↗
PubMed1992

Changes in limbic neuronal function during hormonal induction of lordosis in behaving hamsters.

Several limbic structures influence copulatory behavior and contain receptors for estradiol and progesterone. In the present study, single neuron activity was recorded from septal, amygdaloid, and other limbic regions during the hormonal induction of lordosis in behaving golden hamsters. Limbic neurons had low firing rates and a small number showed firing associated with orienting, sniffing, and rearing. Progesterone administration to estradiol-primed hamsters produced the following neuronal effects: a reduction in the number of active neurons and narrowing of dynamic activity range; enhanced neuronal responsiveness to face stimulation; and lordosis-correlated firing, consisting of depressed activity during lordosis and increased firing at response onset or offset. Unlike previously studied midbrain and hypothalamic neurons, control progesterone injections that didn't produce lordosis were about as effective in altering limbic neuronal activity levels and sensory responsiveness as behaviorally effective injections. The progesterone effects on limbic neurons are consistent with previous evidence suggesting that these neurons tend to suppress lordosis. The significance of these results to hormone influences on epilepsy is discussed.

Animals↗
PubMed1992

Effects of anterior roof deafferentation on lordosis behavior and estrogen receptors in various brain regions of female rats.

This study investigated whether the estrogen receptors (ER), located at different brain areas and anterior pituitary (AP), changed after anterior roof deafferentation (ARD), and on the effects of facilitating the lordosis reflex in female rats. Female rats were ovariectomized and implanted with estradiol capsules. ARD or sham operation was performed with a Halász knife. All animals were tested for lordosis both before and after surgery. One day after the last test they were sacrificed. Cytosol and nuclear ER in the AP, medial preoptic area (MPOA), basal medial hypothalamus (BMH), amygdala (AMYG), septum (SEP), hippocampus (HPC), and cortex (CTX) were measured using an in vitro exchange assay. Rats with ARD showed significantly higher mean levels of lordosis quotient than the control and the sham groups before ARD surgery. An increase of both cytosol and nuclear ER in the BMH area compared to the control was observed, whereas the ER, in the SEP was reduced. ER in other areas were not affected by ARD. Serum estradiol and progesterone levels were not altered by the operation. These data suggest that the dorsal inhibitory pathway from the extrahypothalamus to the preoptic area and hypothalamus may modulate the estrogen receptor and the display of lordosis in female rats. Change of ER level in the BMH area may influence the hormonal sensitivity of lordosis in female rats.

Animals↗
PubMed1993

Lordosis response components can be elicited in decerebrate rats by combined flank and cervix stimulation.

Previous research has indicated that chronically decerebrate adult female rats are incapable of exhibiting lordosis in response to lumbosacral somatic stimuli, suggesting a dependency of this response on forebrain influence. Since vaginocervical stimulation facilitates lordosis to lumbosacral stimuli in rats, the present study investigated the possibility that chronically decerebrate rats could show lordosis in response to flank palpation if vaginocervical pressure was applied concurrently. Six of nine ovariectomized, decerebrate rats exhibited a coordinated display of lordosis-like responses to flank palpation if this stimulus was accompanied by vaginocervical stimulation, but not in response to flank and perineal pressure alone. Estradiol-progesterone treatment increased the magnitude of the response in five of six animals. As in intact rats, cervix pressure in the decerebrates also produced immobilization and blocked responses to nociceptive stimuli. Thus, the caudal neuraxis can mediate expression of essential components of the lordosis response in the absence of forebrain influence.

Animals↗
PubMed1978

Facilitation of lordosis behavior by clonidine in female guinea pigs.

Lordosis behavior was induced in previously unreceptive, ovariectomized estrogen-primed female guinea pigs by administration of the noradrenergic agonist clonidine. Clonidine also enhanced lordosis responding in females that were weakly receptive after estrogen priming. Unlike progesterone, the lordosis-facilitating effect of clonidine was not accompanied by a subsequent refractory period. Clonidine had a weak lordosis facilitatory effect when administered during the decline in receptivity to estrogen plus progesterone-primed animals and failed to induce lordosis when administered during the refractory period.

Animals↗
PubMed1980

Effects of dexamethasone, corticosterone, and ACTH on lordosis in ovariectomized and adrenalectomized-ovariectomized rats.

The involvement of the pituitary-adrenocortical axis in the control of the lordosis reflex was investigated; In Experiment 1, estrogen-primed ovariectomized (ovx) and adrenalectomized-ovariectomized (adx-ovx) females were treated chronically with dexamethasone, a compound blocking ACTH release from the pituitary. Dexamethasone inhibited lordosis, effectively blocking an adrenalectomy-induced facilitation of the reflex. In Experiment 2, corticosterone was similarly administered chronically; this compound also inhibited lordosis in adx-ovx females. In Experiment 3, acute peripheral administration of synthetic ACTH caused a marked increase in lordosis in ovx females. The results suggest that in the adrenally intact animal, ACTH may exert its effect through adrenal steroids. An acute elevation of adrenal steroids may increase lordosis, whereas a chronic elevation may decrease it.

Adrenalectomy↗
PubMed1985

Potentiative action of alpha- and beta-adrenergic receptor stimulation in inducing lordosis behavior.

Ovariectomized (OVX) and ovariectomized-adrenalectomized (OVX-ADX) rats were injected with estradiol benzoate (EB, 4.0 micrograms/rat) and received 44 hr by infusion into the ventromedial hypothalamic area one of the following treatments: norepinephrine (NE), clonidine (an alpha-agonist), isoproterenol (a beta-agonist) or a combination of clonidine and isoproterenol. Infusion of NE (200 ng/rat) induced lordosis in both OVX and OVX-ADX rats 15 minutes after its administration. NE-induced lordosis was blocked by systemic treatment with either the alpha-antagonist, prazosin (1.0 mg/kg), or the beta-antagonist, propranolol (4.0 mg/kg). Intrahypothalamic infusion of clonidine (200 ng/rat) or isoproterenol (200 ng/rat) induced lordosis behavior in OVX, but not in OVX-ADX rats, suggesting the involvement of adrenal secretions in this response. Combined administration of clonidine (100 ng/rat) and isoproterenol (100 ng/rat) induced lordosis behavior 15 minutes after its intrahypothalamic infusion in OVX-ADX animals. Results are discussed in relation to a model proposed for the induction of lordosis behavior involving steroid-NE interactions.

Adrenalectomy↗
PubMed1989

Phorbol esters and forskolin infused into midbrain central gray facilitate lordosis.

Several peptides, when infused into the MCG, facilitate lordosis in estrogen-primed female rats. Since these peptides can act through cAMP and/or protein kinase C, and these second messenger systems have been implicated in neuromodulation, this study examined if pharmacological agents which stimulate these systems would facilitate lordosis. Ovariectomized female Fisher rats were given bilateral cranial cannulae targeted to the MCG, or cortex dorsal to MCG, and allowed at least a week to recover. Forty-eight hours after injection of 1.25 micrograms estradiol benzoate (EB), 1 microliter of each of the following was infused into the MCG (n=8-12): 1) forskolin (5 micrograms/microliter 50% DMSO); 2) phorbol-20-oxo-20-deoxy-12,13-dibutyrate (PBu; 5 micrograms/microliter 50% DMSO); 3) both forskolin and PBu (2.5 micrograms of each/microliter); 4) vehicle (50% DMSO). In a separate study of identical design, 1 microliter of another phorbol ester (12-myristate 13-acetate) was infused into the MCG of EB-primed rats. Forskolin and phorbol esters each facilitated lordosis maximally at 60-90 minutes after infusion. Combining both agents also facilitated lordosis, and vehicle had no effect. These results suggest that infusing agents which stimulate cAMP and protein kinase C into the MCG can facilitate lordosis in estrogen-primed female rats.

Animals↗
PubMed1991

Noradrenergic innervation to the VMN or MPN is not necessary for lordosis.

The purpose of the present study was to determine the importance of noradrenergic neurons terminating in the ventromedial nucleus (VMN) and medial preoptic nucleus (MPN) of the hypothalamus for lordosis behavior in ovariectomized, estrogen/progesterone-treated female rats. Seven days following bilateral injections of the noradrenergic neurotoxin 5-amino-2,4-dihydroxy-alpha-methylphenylethylamine (5-ADMP) into the ventral noradrenergic bundle (VNAB), norepinephrine (NE) concentrations (ng/mg protein) were reduced to 30-35% of control in the VMN and MPN. 5-ADMP-induced lesions of the VNAB also reduced lordosis quotients in these animals, and this effect was reversed by intracerebral ventricular administration of the alpha 1-adrenergic receptor agonist phenylephrine. These results indicate that neurotoxin-induced disruption of noradrenergic neurons in the VNAB is associated with a deficit in sexual receptivity in female rats. To determine if the reduction in sexual receptivity following 5-ADMP-induced lesions of the VNAB resulted from loss of noradrenergic neuronal projections specifically to the VMN or MPN, lordosis quotients were determined in ovariectomized, estrogen/progesterone-treated rats in which noradrenergic terminals in these hypothalamic nuclei were selectively lesioned. Injection of 5-ADMP directly into either the VMN or MPN reduced NE concentrations to 17% of control in these hypothalamic nuclei, but failed to alter lordosis. Furthermore, injection of phenylephrine into either the VMN or MPN of VNAB-lesioned rats failed to reinstate lordosis to the levels comparable to sham-lesioned controls. Taken together, these results indicate that noradrenergic neurons terminating in either the VMN or MPN are not essential for gonadal steroid induction of sexual receptivity in ovariectomized female rats.

Animals↗
PubMed1987

Oxytocin-induced facilitation of lordosis behaviour in rats is progesterone-dependent.

Oxytocin was administered intracerebroventricularly to ovariectomized female rats and its effect on lordosis was examined. In Experiment 1a, oxytocin (0.17 mU in 4 microliters saline) failed to facilitate lordosis behaviour in animals primed acutely with 10 micrograms estradiol benzoate (EB) and 300 micrograms progesterone (P). In Experiment 1b, however, oxytocin significantly facilitated lordosis in animals primed acutely with 10 micrograms EB and 250 or 200 micrograms P. In Experiments 2a and 2b, oxytocin failed to facilitate lordosis in animals treated acutely with 10 micrograms EB, or chronically with 0.8 micrograms EB daily for eight days prior to testing. These results support the hypothesis that the facilitation of lordosis in ovariectomized rats by centrally-administered oxytocin is progesterone-dependent.

Animals↗
PubMed1985

Effects of septal lesion on lordosis response induced by estradiol in middle-aged and old female rats.

Long-Evans female rats were divided into three age groups: 10 young rats (5 months of age), 7 middle-aged rats (10-13 months of age) and 6 old rats (21-27 months of age). The rats were ovariectomized and immediately implanted subcutaneously with a silastic capsule filled with estradiol benzoate (E2). Lordosis response was compared in each animal before and after the septal lesion. Serum E2 levels were 197 +/- 27 pg/ml (mean +/- SEM), 192 +/- 81 pg/ml and 405 +/- 83 pg/ml in young, middle-aged and old rats respectively. When serum E2 levels were adjusted by analysis of covariance, LQ (lordosis quotient) was 42, 36 and 61 in young, middle-aged and old rats respectively before the septal lesion and 98, 68 and 88 respectively after the septal lesion. The extent of potentiation of lordosis after the septal lesion was less in middle-aged and old rats than young rats. These results indicate that an enhanced lordosis response in aged rats is partly due to high circulating E2 levels and partly due to disinhibition of the septal region on lordosis.

Aging↗
PubMed1991

Excitatory amino acid modulation of lordosis in the rat.

Microinfusion of the excitatory amino acid agonist N-methyl-D-aspartate (NMDA) into the mediobasal hypothalamus (MBH) significantly reduced lordosis in estrogen plus progesterone-treated female rats at 10 min post-infusion with recovery to pretest values by 30 min (P less than .05; Wilcoxon). Microinfusion of the specific NMDA antagonist D,L2-amino-5-phosphonopentoic acid (AP-5) into the same sites was without effect on lordosis responding of fully receptive females. There was also a significant increase in the number of females vocalizing to mounts by males after infusion of NMDA but not after infusion of AP-5 into the MBH. When NMDA was infused into the preoptic area (POA) there was no effect on lordosis responding of full receptive females, but AP-5 infusion resulted in a significant inhibition of lordosis at 10 min post-infusion. There was no difference between groups in percentage of females vocalizing after drug infusion into the POA. These results suggest that increased excitatory amino acid activity in the MBH and decreased excitatory amino acid activity in the POA inhibits lordosis behavior.

2-Amino-5-phosphonovalerate↗