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PubMed1977

Examination of some factors that control the effects of septal lesions on lordosis behavior.

Various experimental parameters related to the effects of septal lesions on the lordosis behavior of rats have been examined. First, the failure of septal lesions to facilitate lordosis behavior in male rats appears to be related to the degree of exposure to androgens neonatally. The normal facilitation in lordosis behavior associated with septal destruction in adult female rats does not occur if these female rats are treated with 1.0 mg of testosterone propionate (TP) on Day 1 of life. Yet female rats given 270 mug of TP on Day 3 of life respond the same as do normal females to septal lesions. Second, these sexually dimorphic effects of septal lesions can be modified in adult rats by chronic treatment with gonadal hormones following septal destruction. Whereas previous studies indicated that chronic estrogen injections permit a facilitation in lordosis behavior to occur in septal lesioned male rats, the present results showed that chronic injections of TP following a septal lesion attenuates the facilitation in lordosis behavior typically observed in adult female rats following a septal lesion. Third, examination of the time course for the facilitation in lordosis behavior following a septal lesion revealed a four to six day delay before the appearance of heightened female sexual behavior. Fourth, in support of the possibility that modifications in lordosis behavior by septal lesions may be mediated by a depletion or imbalance in brain amines, amphetamine was found to reduce the high levels of lordosis behavior of septal lesioned female rats to control levels. Finally, further evidence of a potential role for brain amines in the effects of septal lesions was provided by the observation of significantly lower content and turnover of dopamine in the amygdala of septal lesioned female rats, relative to sham operated controls.

Animals↗
PubMed1988

Stimulation of beta-adrenoceptors inhibits lordosis behavior in the female rat.

Existing reports on the effects of beta-adrenergic antagonists on lordosis behavior appear contradictory, with (+/-) propranolol being reported to inhibit, and (+/-) pindolol to facilitate this behavior. In the present study, both the (-) and (+) optical isomers of propranolol were effective in inhibiting lordosis behavior in ovariectomized rats treated with estrogen and progesterone. This finding suggests that the lordosis-inhibiting effects of propranolol were not due to blockade of beta-adrenergic activity, but rather to the membrane stabilizing effect of the drug. An observed inhibition of lordosis following the peripheral administration of the local anesthetic lidocaine is consistent with this possibility. (+/-) Propranolol had no effect 30 min after peripheral administration in estrogen-treated, ovariectomized rats with low baseline levels of lordosis behavior. (+/-) and (-) pindolol, but not (+) pindolol also inhibited lordosis 30 min after administration. However, in addition to its antagonist effects, pindolol acts as a partial agonist in some tissues. Centrally active doses of the pure beta-antagonist (+/-) metoprolol produced no inhibitory effects. Indeed, metoprolol reversed the inhibitory effect of the beta-agonist (+/-) salbutamol. This suggests that the lordosis-inhibiting effects of pindolol were due to its partial agonist effects. Taken together, the present data indicate that activity at central beta-adrenoceptors inhibits rather than facilitates lordosis behavior.

Animals↗
PubMed1988

Blockade of LHRH-induced lordosis by alpha- and beta-adrenergic antagonists in ovariectomized, estrogen primed rats.

The participation of a noradrenergic mechanism in the facilitation of lordosis by luteinizing hormone-releasing hormone (LHRH) was studied in two groups of ovariectomized estrogen primed rats, with or without sexual experience. The administration of 5 micrograms estradiol benzoate (EB) alone to sexually inexperienced subjects (Ss) induced weak lordosis behavior in some of them (mean lordosis quotient, LQ = 12 +/- 19). The SC injection of 5 micrograms LHRH significantly increased this response four hours later (LQ = 38 +/- 41), though great variability was observed (59% of Ss showing LQs below 30). The systemic administration of either prazosin, an alpha-adrenergic antagonist (0.2 or 1 mg/kg), or propranolol, a beta-adrenergic antagonist (20 mg/kg), totally suppressed LHRH-induced lordosis in sexually inexperienced Ss (mean LQs = 8 +/- 11; 5 +/- 10; 18 +/- 31, respectively). In sexually experienced Ss (tested on two previous occasions with EB and LHRH) the administration of EB alone on a third test induced significant levels of lordosis (mean LQ = 51 +/- 41). The administration of 5 micrograms LHRH to sexually experienced, estrogen primed Ss induced near maximal levels of lordosis (LQ = 94 +/- 18). In these Ss, prazosin (0.2 and 1 mg/kg) and, to a lesser extent, propranolol (20 mg/kg) significantly depressed lordosis to values that were not significantly different from those obtained after EB alone (mean LQs = 59 +/- 38; 63 +/- 20; 74 +/- 32, respectively). These results indicate that blockade of noradrenergic transmission by either alpha- or beta-antagonists counteracts the stimulatory effect of LHRH on lordosis in ovariectomized estrogen primed rats with or without sexual experience.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1989

Alpha 1 noradrenergic antagonism decreases hormonally-induced and hormonally-independent lordosis.

Manipulations of the alpha noradrenergic (NE) system affect both lordosis and the concentration of hypothalamic steroid receptors. The present studies explored whether NE affects lordosis in guinea pigs via changes in hypothalamic estrogen or progestin receptors or through some other mechanism. The alpha 1 NE antagonist prazosin blocked lordosis which was induced with estradiol benzoate (EB) followed by progesterone (P), lordosis which was induced by EB alone and lordosis which is not dependent upon gonadal hormones for its display. These results suggest that NE modulation of lordosis in the guinea pig is not exerted solely through progestin receptors or estrogen receptors. Because prazosin blocked hormonally-independent lordosis, it is apparent that the NE system modulates some nonhormonal component of lordosis in guinea pigs.

Animals↗
PubMed1989

Different roles of alpha-noradrenergic receptor subtypes in regulating lordosis.

Ovariectomized guinea pigs were given free estradiol (E) at hr 0 and 28, and progesterone (P) at hr 39. Experiment 1: The alpha-1 noradrenergic antagonist prazosin, but not the alpha-2 noradrenergic antagonist idazoxan, prevented display of lordosis behavior when administered systemically 30 min prior to E injections at either hr 0 or 28, or 30 min prior to both injections. Experiment 2: Multiple injections of idazoxan (i.e., 30 min prior to and 60 and 120 min after each E injection) failed to prevent display of lordosis. Experiment 3: E-primed animals were given a single injection of idazoxan 1 hr before P, or 5 hr after P. In those animals given idazoxan 1 hr before P, display of lordosis was not prevented. However, in animals given idazoxan once lordosis display had begun (i.e., 5 hr after P) ongoing lordosis behavior was blocked. These data suggest differential roles of alpha-noradrenergic receptor subtypes in regulation of lordosis: noradrenergic transmission through the alpha-1 subtype may mediate hormone-priming processes leading to lordosis, whereas transmission through the alpha-2 subtype may modulate ongoing lordosis responses.

Adrenergic alpha-Antagonists↗
PubMedDate not supplied

Selective activation of opioid receptors differentially affects lordosis behavior in female rats.

The effects of opioid peptides that are highly selective ligands for mu receptors (morphiceptin). delta receptors (delta-receptor peptide), kappa receptors (dynorphin 1-9), and the mu/delta complex (beta-endorphin), were tested on lordosis behavior in ovariectomized rats primed with estrogen and progesterone. Intracerebroventricular infusions of beta-endorphin or morphiceptin both inhibited and facilitated lordosis in a dose-dependent fashion whereas all doses of delta-receptor peptide facilitated lordosis. Dynorphin 1-9 had no significant effect at any dose, although a trend toward increased lordosis quotients was observed 30 min after infusion. The effects of beta-endorphin, morphiceptin, and delta-receptor peptide were reversed with naloxone, although naloxone alone had no effect on lordosis behavior. These results indicate that the specific activation of opioid receptor subtypes differentially affects lordosis behavior. It appears that binding to high-affinity mu 1 receptors exerts an inhibitory influence on lordosis, whereas binding to low-affinity mu 2 receptors or delta receptors exerts a facilitatory influence. Binding to kappa receptors does not appear to affect lordosis behavior.

Angiotensin II↗
PubMed1999

5-HT2C receptor involvement in female rat lordosis behavior.

Adult, hormone-primed, ovariectomized rats (CDF-344) with bilateral implants within the ventromedial nucleus of the hypothalamus (VMN), were injected with 0.5 microgram estradiol benzoate followed 48 h later with 500 microgram progesterone. This priming produced rats with 2 different levels of sexual receptivity. Rats with a lordosis to mount ratio (L/M)>/=0.5 were used to examine the potential lordosis-inhibiting effects of the 5-HT2A receptor antagonist, R(+)-a-(2, 3-dimethoxyphenyl)-1-[2(4-fluoro-phenylethyl)]-4-piperidine-methanol (MDL 100,907), and the 5-HT2C receptor antagonist, 5-methyl-1-(3-pyridylcarbamoyl)-1,2,3,5-tetrahydropyrrolo[2, 3-f]indole (SB 206553). Rats with low sexual receptivity (L/M<0.5) were bilaterally infused with the 5-HT2A/2C receptor agonist, (+/-)-1-(2,5-dimethoxy-4-iodophenyl)-2-aminopropane HCl (DOI), or DOI plus either MDL 100,907 or SB 206553 to determine if either drug would attenuate the lordosis-facilitating effects of DOI. The 5-HT2C receptor antagonist, but not the 5-HT2A receptor antagonist, effectively inhibited lordosis behavior. Similarly, SB 206553 was more effective than MDL 100,907 in reducing the DOI-induced increase in lordosis responding. However, both drugs limited the duration of lordosis responding initiated by DOI. These results are consistent with prior suggestions that 5-HT2A/2C receptors within the VMN are involved in the modulation of lordosis behavior and lead to the suggestion that 5-HT2C, rather than 5-HT2A, receptors are primarily responsible for the effects of 5-HT2 receptor-active drugs on lordosis behavior.

Animals↗
PubMed2000

Anti-sense oligonucleotides, for progestin receptors in the VMH and glutamic acid decarboxylase in the VTA, attenuate progesterone-induced lordosis in hamsters and rats.

Immunocytochemical (ICC) staining for progesterone (P) receptors (PRs) and glutamic acid decarboxylase (GAD), the enzyme responsible for GABA production, reveal that there are many PRs in the ventral medial hypothalamus (VMH) and many GAD containing neurons in the ventral tegmental area (VTA). To investigate P's action on lordosis in the VMH and VTA, anti-sense oligos specific to PRs and GAD(65&67) were intracerebrally infused into the VMH and VTA of 24 ovariectomized hamsters and 40 ovariectomized rats. Estradiol benzoate (2 microg) primed hamsters and rats were infused to the VMH and the VTA with either PR (250 ng/1.0 microl infusion) or GAD (500 ng/1.0 microl infusion) anti-sense oligos, their scramble controls, or saline vehicle at hour 0 and again at hour 24. At hr 44, rodents were subcutaneously injected with P (500 microg) and were tested for sexual receptivity with a male 4 h later. There were significant reductions in lordosis of hamsters and rats following PR anti-sense infusions to the VMH compared to scrambled or vehicle control infusions. Effects of PR anti-sense to the VMH were not different from combined VMH and VTA PR anti-sense infusions; however, VMH infusions reduced lordosis compared to VTA-only anti-sense infusions. GAD anti-sense infusions reduced lordosis when infused into the VTA, compared to scrambled or saline vehicle infusions. Lordosis responsiveness following VTA GAD anti-sense infusions was not different from combined VMH and VTA infusions, but VTA infusions of GAD anti-sense reduced lordosis compared to VMH-only anti-sense infusions. These data suggest that in the VMH, PRs are important for P-facilitated lordosis, whereas in the VTA, GABAergic neurons may be an important substrate for mediating P's actions on lordosis of rodents.

Animals↗
PubMed2002

The role of delta-opioid receptors in estrogen facilitation of lordosis behavior.

The present study investigated the role of delta-opioid receptors (ORs) in estrogen facilitation of female rat reproductive behavior (lordosis). Infusion of 2 microg of the selective delta-OR agonist [D-Pen(2),D-Pen(5)]-enkephalin (DPDPE), into the third ventricle facilitated lordosis behavior in ovariectomized (OVX) rats injected with estrogen (E) 48 and 24 h before behavioral testing. Pretreatment with the selective delta-OR antagonist naltrindole (NTDL) blocked DPDPE effects on lordosis behavior. Ventricular infusion of NTDL (40 microg) also suppressed lordosis behavior in fully receptive OVX rats primed with both E and progesterone (P). In addition, NTDL blocked lordosis behavior when infused into the ventromedial nucleus of the hypothalamus (VMH) but not into the medial preoptic area (mPOA). Site-specific infusion of DPDPE into the VMH had dose-dependent, dual effects on lordosis behavior. While a very low dose of DPDPE (0.01 microg) facilitated lordosis behavior, a higher dose (1.0 microg) inhibited receptivity in OVX rats primed with E and a low dose (50 microg) of P. We used 3H-DPDPE to measure the density of delta-ORs in OVX rats treated with vehicle or with E by receptor autoradiography. E treatment did not have any effect on the density of DPDPE binding sites in the VMH, mPOA, medial amygdala, or caudate putamen. The behavioral effects of the ligands used in this study suggest that activation of delta-OR in the VMH by endogenous opioids facilitates estrogen-dependent lordosis behavior.

Analgesics, Opioid↗
PubMed1977

Somatosensory determinants of lordosis in female rats: behavioral definition of the estrogen effect.

By coating the ventral surface of male rats with a dye, regions of contact between male and female during male mounting were recorded precisely on the female's hair and skin. The male rat touches the female's flanks, rump, tailbase, perineum, and perivaginal surfaces during the female's initiation and maintenance of lordosis. Film analyses showed that the male's paws and pelvic thrusting stimulate the female's skin with dominant frequencies between 10 and 20 per second. Somatosensory stimuli were applied by the experimenter to the female skin locations contacted by the male. Deflection of hair on the flanks or perineum alone did not cause lordosis. Light stimulation simultaneously on flanks and perineum caused lordosis only in some females given high estrogen dosages supplemented by progesterone. When flank stimuli were followed by pressure on the rump, tailbase, and perineum, lordosis was triggered reliably in hormone-treated females. Here the estrogen-dependence of the reflex was shown, and progesterone synergized with the estrogen effect. Among lordosis components, rump and head elevations in response to pressure stimuli on the rump, tailbase, and perineum appear to be hormone-sensitive. These results help to define the minimal cutaneous sensory requirement for lordosis. In turn, the estrogen effect on lordosis may be defined behaviorally as increased responsiveness to pressure on rump, tailbase, and perineal skin, after flank stimulation. These results illustrate how estrogen, progesterone, and somatosensory stimuli interact in causing lordosis, increases in the strength of one factor compensating for decreases in another.

Animals↗
PubMed2005

Inhibiting biosynthesis and/or metabolism of progestins in the ventral tegmental area attenuates lordosis of rats in behavioural oestrus.

In the ventral tegmental area (VTA), lordosis of rats is facilitated by 5alpha-pregnan-3alpha-ol-20-one (3alpha,5alpha-THP). Central 3alpha,5alpha-THP results from metabolism of peripheral progesterone, from the ovaries and/or adrenals, by sequential enzymatic activity of 5alpha-reductase and 3alpha-hydroxysteroid oxidoreductase (3alpha-HSOR). In addition, in glial cells, cholesterol is converted into pregnenolone by the P450 side-chain cleavage enzyme (P450scc), which is then metabolized to progesterone by 3beta-hydroxysteroid dehydrogenase, and subsequently reduced to 3alpha,5alpha-THP. We hypothesize that, in the VTA, formation of 3alpha,5alpha-THP by both metabolism and biosynthesis is necessary for facilitation of lordosis of female rats. In Experiment 1, naturally-receptive rats received bilateral VTA infusions of a P450scc inhibitor, digitoxin (1 microg/side); a 5alpha-reductase inhibitor, finasteride (10 microg/side); digitoxin (1 microg/side)+finasteride (10 microg/side); or vehicle and were tested 3 h later for lordosis. In Experiment 2, the effects of VTA infusions of digitoxin, finasteride, digitoxin+finasteride, or vehicle on lordosis and midbrain and plasma 3alpha,5alpha-THP levels were examined. In Experiment 3, we investigated whether infusions of 3alpha,5alpha-THP to the VTA reinstated lordosis and midbrain 3alpha,5alpha-THP levels following administration of inhibitors. VTA infusions of digitoxin, finasteride, or digitoxin+finasteride, significantly and similarly reduced lordosis and midbrain, but not plasma 3alpha,5alpha-THP levels, compared to vehicle. Following receipt of inhibitor infusions, 3alpha,5alpha-THP to the VTA restored lordosis and midbrain 3alpha,5alpha-THP levels. These data suggest that, in the VTA, both central biosynthesis of progesterone and metabolism of progesterone (from central and/or peripheral sources) to 3alpha,5alpha-THP are important for mediating lordosis of rats.

Animals↗
PubMed2006

In the ventral tegmental area, cyclic AMP mediates the actions of progesterone at dopamine type 1 receptors for lordosis of rats and hamsters.

Progesterone-facilitated lordosis is enhanced by activation of, and inhibited by antagonism of, dopamine type 1 receptors (D1) in the ventral tegmental area (VTA). Given that D1 activation leads to increases in cyclic AMP (cAMP), we hypothesised that, in the VTA, progesterone's actions on lordosis that involve D1 are mediated, in part, by cAMP. In Experiment 1, naturally receptive rats and hamsters were pretested for lordosis, infused with the cAMP analogue 8-bromo-cAMP (200 ng) or vehicle to the VTA, and tested again 30 min later. In Experiments 2 and 3, ovariectomised, oestradiol (10 microg) + progesterone (0 or 100 microg)-primed rats and oestradiol (10 microg) + progesterone (0 or 200 microg)-primed hamsters were pretested for lordosis and infused with 8-bromo-cAMP (200 ng), the adenylyl cyclase inhibitor 2',5'-dideoxyadenosine (12 microM) or vehicle to the VTA. Subjects were tested again 30 min later. In Experiment 4, oestradiol + progesterone-primed rats and hamsters were pretested and infused with the D1 agonist SKF38393 (0 or 100 ng) to the VTA. Thirty minutes later, subjects were tested again and infused with 2',5'-dideoxyadenosine (12 microM) or vehicle. Subjects were tested again 30 min later. VTA infusions of 8-bromo-cAMP enhanced lordosis of naturally receptive or hormone-primed rats and hamsters and 2',5'-dideoxyadenosine decreased lordosis of oestradiol + progesterone-primed rats and hamsters. D1-mediated increases in progesterone-facilitated lordosis were reduced by 2',5'-dideoxyadenosine. These data suggest that progesterone-facilitated lordosis of rats and hamsters may be modulated by D1 and cAMP activity in the VTA.

Analysis of Variance↗
PubMed2003

Lumbar lordosis: study of patients with and without low back pain.

We used magnetic resonance imaging (MRI) to assess lumbar lordosis in 27 patients with low back pain and 19 patients and 10 volunteers with no known back pain. Our study aimed to investigate whether lordosis changes with age and is reduced in those with low back pain. Although our results confirm known observations that lumbar lordosis is more prominent in women (P < 0.01) and those with a higher body mass index (P < 0.04), we were unable to demonstrate any significant variation in lordosis with age. Nor could we demonstrate any difference in the degree of lordosis among women with or without back pain. Men with low back pain tended to have a less prominent lordosis, but this difference did not reach statistical significance. Therefore, a 'reduced lumbar lordosis' should be regarded as a very weak clinical sign.

Adult↗
PubMed1989

A comparison of actual and apparent lumbar lordosis in black and white adult females.

The purposes of this study were to investigate differences in lumbar lordosis in black and white adult females and to explain the clinical impression that blacks have a greater lordosis than whites. An actual lumbosacral lordosis angle (ALS) was measured from a standing right lateral lumbosacral radiograph using the angle formed from the intersection of lines drawn across the top of the second lumbar vertebral body (L2) and across the top of the sacrum. An actual lumbo-lumbar angle (ALL) was measured in the same manner, except the second line was drawn across the bottom of the fifth vertebral body (L5). To determine whether gluteal prominence gives a false impression of increased lumbar lordosis, an apparent lordosis (APL) measurement was taken, measuring the distance from the subject's greater trochanter to the most posterior aspect of the buttocks. No significant differences were found in ALS or ALL between 25 black and 27 white adult female subjects (ALS, P = 0.26; ALL, P = 0.41). Significant differences were found between black and white APL, with blacks demonstrating a larger APL than whites (P less than 0.01). A high correlation was noted between ALS and ALL in both blacks (0.70, P less than 0.01) and whites (0.77, P less than 0.01). The investigators therefore contend that the clinician's assumption that blacks have a greater lordosis than whites is based on an apparent increased lordosis due to more prominent buttocks (APL).

Adolescent↗
PubMed1975

Action of luteinizing hormone-releasing factor (lrf) in the initiation of lordosis behavior in the estrone-primed ovariectomized female rat.

In order to evaluate the precise role of luteinizing hormone-releasing factor (LRF) in mediating the onset of sexual behavior, the specificity, time-course, and dose-response relationship of LRF-facilitated lordosis behavior were determined. Ovariectomized female rats, pretreated with estrone and LRF, displayed a pattern of lordosis behavior which differed little from that produced by estrone-progesterone. Little if any lordosis behavior was observed in response to LRF alone, estrone alone, or estrone in combination with luteinizing hormone (LH), follicle-stimulating hormone (FSH), or thyrotropin-releasing factor (TRF). Furthermore, LRF-induced lordosis behavior occurred in the absence of the adrenals, thus eliminating adrenal progesterone as a factor in facilitating the appearnce of lordosis behavior. The LRF-facilitated lordosis behavior was seen 2 h after the injection of LRF and was maintained for a total of 8 h. A minimal dose of 150 ng LRF was required to initiate the first consistent appearance of lordosis behavior; the maximum response was obtained with 500 ng. It is thus suggested that LRF is not only responsible for the ovulatory discharge of LH and subsequent ovulation, but may also play a role in the initiation of the onset of mating behavior in the female rat.

Adrenal Glands↗
PubMed1998

Site-specific opioid receptor blockade allows prepubertal guinea pigs to display progesterone-facilitated lordosis.

Ovariectomized (OVX) juvenile guinea pigs (approximately 3 weeks old) rarely display steroid-induced sexual receptivity. Systemic administration of the opioid receptor antagonist naloxone enhances the display of progesterone-facilitated lordosis in prepubertal females, suggesting that endogenous opioids tonically inhibit the expression of sexual receptivity at this age. This study was designed to ascertain the neural site(s) at which naloxone injection would stimulate lordosis in juvenile guinea pigs. Hartley guinea pigs were OVX at 10-11 days of age and 2-6 days later implanted with bilateral cannulae aimed at the medial preoptic area/anterior hypothalamus (MPOA/AH), ventrolateral hypothalamus/ventromedial hypothalamus (VLH/VMH), or mesencephalic central gray (MCG). At 21-23 days of age, following administration of estradiol benzoate (10 microgram(s)) and progesterone (0.5 mg), naloxone (100 ng/side) or 0.9% saline was injected through the cannulae and the guinea pigs were tested for the display of lordosis. The MPOA/AH was the only site at which application of naloxone reliably elicited lordosis (87% positive response vs 12% for saline). Few females (< 17%) displayed lordosis following injections of naloxone or saline into the VLH/VMH or MCG. A second experiment demonstrated that the stimulation of lordosis following MPOA/AH naloxone application was prevented by prior injection of the opioid agonist morphine (500 ng/side) at the same site. These data support the hypothesis that endogenous opioids acting in the MPOA/AH, but not the VLH/VMH or MCG, tonically inhibit the display of progesterone-facilitated lordosis in prepubertal guinea pigs.

Animals↗
PubMed2002

Activation of mu-opioid receptors inhibits lordosis behavior in estrogen and progesterone-primed female rats.

The present study investigated the effect of highly selective mu-opioid receptor (OR) agonists on lordosis behavior in ovariectomized rats treated with 3 microg of estradiol benzoate followed 48 h later by 200 microg of progesterone. Ventricular infusion of the endogenous mu-OR agonists endomorphin-1 and -2 suppressed receptive behavior in a time- and dose-dependent fashion. At 6 microg, both endomorphin-1 and -2 inhibited lordosis behavior within 30 min. However, while the effect of endomorphin-1 lasted 60 min, endomorphin-2 inhibition lasted up to 120 min after infusion. Pretreatment with naloxone (5 mg/kg sc) was able to block both endomorphin-1 and endomorphin-2 effects on lordosis. Site-specific infusions of endomorphin-1 or endomorphin-2 into the medial preoptic area (mPOA), the ventromedial nucleus of the hypothalamus (VMH), or into the mesencephalic central gray did not affect receptivity. In contrast, infusion of 1 mug of either compound into the medial septum/horizontal diagonal band of Broca inhibited lordosis in a pattern very similar to that seen after intraventricular infusions. Infusion of the potent synthetic mu-OR agonist [D-Ala(2),N-Me-Phe(4),Gly-ol(5)]-enkephalin (0.08 microg) into the VMH and mPOA inhibited lordosis behavior for at least 60 min after infusion. The nonspecific opioid receptor antagonist naloxone was able to facilitate lordosis in partially receptive female rats when infused into the mPOA but not when infused into the VMH. The behavioral effects of the agonists and antagonist used in this study suggest that the endogenous mu-opioid system modulates estrogen and progesterone-induced lordosis behavior.

Analgesics, Opioid↗
PubMed1977

Effects of spinal cord transections on lordosis reflex in female rats.

(1) Female rats with complete transections of spinal cord at low thoracic levels were not able to perform the lordosis reflex. (2) Females with bilateral transections of dorsal columns, dorsolateral columns or entire dorsal half of spinal cord performed lordosis in a normal way. (3) Bilateral transection of fibers in the ventromedial columns, added to transection of dorsal columns or entire dorsal half of the cord still allowed lordosis to be performed. (4) Large bilateral transections of the anterolateran columns caused severe loss in the strength and frequency of the lordosis reflex. Effective transections often included some ventromedial or dorsolateral column fibers, and were accompanied by abnormalities of locomotion. (5) We conclude that supraspinal control is required for the normal lordosis reflex, and that fibers necessary and sufficient for lordosis run in the anterolateral columns. These fibers are likely to be dispersed throughout the anterolateral columns, since large transections were required to eliminate lordosis, and also to be involved in (or interspersed with other fibers involved in) other aspects of motor control. Candidate ascending systems are the anterolateral fibers of Mehler. Candidate descending systems are the lateral vestibulospinal and reticulospinal tracts.

Animals↗