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Does anterior plating maintain cervical lordosis versus conventional fusion techniques? A retrospective analysis of patients receiving single-level fusions.

A retrospective review of medical records and radiographs of patients receiving anterior cervical discectomy and fusion (ACDF) without anterior plating and with anterior plating was performed. The objective of the study was to determine whether a difference exists in cervical lordotic alignment between subjects undergoing single-level ACDF with and without anterior cervical plating instrumentation for symptomatic cervical disc disease. Collapse or settling of grafted bone into the vertebral endplates with resulting kyphotic deformity of the cervical spine is a commonly described complication of anterior discectomy and fusion. Despite the increasing use of instrumentation for the treatment of cervical spine injuries and degenerative conditions, little is known regarding lordotic alignment of the cervical spine in patients who receive plating instrumentation compared with conventional fusion without plating. Accumulating evidence suggests that plating is superior to non-plating techniques in patients with multiple level cervical disc lesions in regard to fusion, return to work rates, and complication rates; however, little is known about maintenance of lordotic curve alignment in single- and multiple-level procedures. Neutral lateral cervical radiographs of 57 patients who underwent single-level ACDF between 1994 and 1999 with anterior screw plates (n = 26), and conventional single-level fusion without anterior screw plates (n = 21) were retrospectively assessed. Measurements were made on weight-bearing lateral cervical radiographs to assess overall sagittal spinal alignment and intersegmental sagittal alignment at the surgical site before surgery, immediately after surgery, 4 to 12 weeks after surgery, and 12+ months after surgery. The average magnitude of overall lordosis measured between C2 and C7 decreased 4.2 degrees in the non-plated group, while being preserved in the plated group. This finding did not reach statistical significance in the long-term follow-up. At the surgical site, the segmental contribution to lordosis decreased an average 2.5 degrees in the non-plated group versus an increase of 5.67 degrees in the plated group, and this finding was statistically significant between groups measured at all pre- and postoperative visits (p < 0.01). On average, the plating procedure resulted in preserving overall lordosis while increasing the magnitude of segmental lordosis at the surgical site. In comparison, the conventional method resulted in a net loss of overall lordosis and segmental lordosis at the surgical site.

Analysis of Variance↗

An analysis of sagittal spinal alignment following long adult lumbar instrumentation and fusion to L5 or S1: can we predict ideal lumbar lordosis?

STUDY DESIGN: A retrospective study. OBJECTIVE: To determine factors controlling sagittal spinal balance after long adult lumbar instrumentation and fusion from the thoracolumbar spine to L5 or S1. SUMMARY OF BACKGROUND DATA: To our knowledge, no study on postoperative sagittal balance following long adult spinal instrumentation and fusion to L5 or S1 has been published. METHODS: A clinical and radiographic assessment of 80 patients with adult lumbar deformity (average age 53.4 years) who underwent long (average 7.6 vertebrae, 5-11 vertebrae) segmental posterior spinal instrumentation and fusion from the thoracolumbar spine to the L5-S1 (average 4.5 years, 2-15.8-year follow-up) was performed. We defined the optimal sagittal balance (n = 42) group, the distance from C7 plumb to superior posterior endplate of S1 < or = 3.0 cm, and the suboptimal sagittal balance (n = 38) group, the distance from C7 plumb to superior posterior endplate of S1 > 3.0 cm at ultimate follow-up. RESULTS: The optimal sagittal balance group (C7 plumb, average -0.6 +/- 2.5 cm) had the larger average angle differences between lumbar lordosis and thoracic kyphosis (P < 0.0001), preoperative smaller pelvic incidence (P = 0.007), smaller average thoracolumbar junctional angle (T10-L2) increase (P < 0.0001), and bigger lumbar lordosis angle increase (P = 0.014) at ultimate follow-up. Patients with optimal sagittal balance at ultimate follow-up had significantly higher total Scoliosis Research Society 24 outcome scores than those with suboptimal sagittal balance (P = 0.015). Risk factors that were statistically significant for the suboptimal sagittal balance group included pelvic incidence compared with lumbar lordosis (> or = 45 degrees) before surgery (vs. < 45 degrees, P = 0.009), smaller lumbar lordosis compared with thoracic kyphosis (< 20 degrees) at 8 weeks postoperatively (vs. > or = 20 degrees, P = 0.013), and older than 55 years of age at surgery (vs. 55 years or younger, P = 0.024). CONCLUSION: A sagittal Cobb angle difference between lumbar lordosis and thoracic kyphosis of > 20 degrees (higher lumbar lordosis) is advisable in most circumstances to achieve optimal sagittal balance.

Adult↗

Role of postnatal androgens in sexual differentiation of the lordosis-inhibiting effect of central injections of cholecystokinin.

The neuropeptide cholecystokinin (CCK) inhibits lordosis behavior when infused into the ventromedial nucleus of the hypothalamus (VMN) of female rats and has no effect when infused into the VMN of male rats. To test whether this sex difference develops under the control of perinatal steroids, male rats were castrated or given sham surgeries within 3 h of birth and female rats were injected with either 0 or 100 micrograms testosterone propionate on postnatal day 5. As adults, these rats were castrated as necessary, implanted with unilateral cannulae directed at the VMN, and tested for their ability to display female sexual behavior and to respond to CCK. Neonatal castration of males prevented defeminization of this response. When treated with 5 micrograms estradiol benzoate (EB), neonatally castrated males showed both lordosis behavior and a profound inhibition of that behavior after infusions of CCK. Neonatally castrated males did not display lordosis behavior when treated with 2 micrograms EB. Control males showed no lordosis behavior and, therefore, no response to CCK. Both doses of EB induced lordosis behavior in neonatally androgenized females. Significantly, these neonatally androgenized females were less responsive to CCK's inhibition of lordosis and were also anovulatory. These results imply that androgens alter the development of CCK responsive circuits as well as defeminize cyclic gonadotropin release. Levels of 125I-sCCK-8 binding in the VMN were correlated closely with an individual's ability to respond to sCCK-8. In summary, the inhibition of female sexual behavior caused by exogenously administered CCK in normal adult female rats appears to be controlled at least partially by levels of CCK receptors in the VMN and to differentiate under the control of perinatally present testosterone.

Androgens↗

The role of the uterus and cervix in systemic oxytocin-PGE2 facilitated lordosis behavior.

The effect of ovariectomy, hysterectomy, and cerviectomy on systemic oxytocin-PGE2 induced facilitation of lordosis behavior was examined in estrogen and progesterone treated rats. Females were injected with 0.25 micrograms estradiol benzoate for 3 days, followed by 500 micrograms progesterone on day 4, 4 hr prior to behavioral testing. Ten minutes before behavioral testing with a male, females were injected systemically with either oxytocin (2.1, 4.2, or 8.4 micrograms); PGE2 (0.05, 0.10, or 0.20 micrograms); concomitant administration of both oxytocin and PGE2; or physiological saline. Oxytocin (2.1 micrograms) or PGE2 (0.05 micrograms) significantly increased lordosis behavior in ovariectomized females; however, neither had any facilitatory effect in hysterectomized animals. Facilitated lordosis behavior was only reinstated in hysterectomized females that received concomitant administration of 2.1 micrograms oxytocin plus 0.05 micrograms PGE2. This latter dose also resulted in a further potentiation of lordosis behavior in ovariectomized animals, compared to 2.1 micrograms oxytocin or 0.05 micrograms PGE2 alone. Concomitant administration of oxytocin and PGE2 at all doses had no facilitatory effect on lordosis behavior in cerviectomized animals. These results suggest that the uterus and the cervix may be important components of a peripheral mechanism by which systemic oxytocin and/or PGE2 induce facilitated lordosis behavior in female rats.

Animals↗

Prior treatment with estrogen attenuates the effects of the 5-HT1A agonist, 8-OH-DPAT, on lordosis behavior.

The effects of repeated treatment with estradiol benzoate to ovariectomized rats on the lordosis-inhibiting action of the 5-HT1A agonist, 8-hydroxy-2(di-n-propylamino) tetralin (8-OH-DPAT), were examined. In the first week of hormonal priming, when rats were injected with estradiol benzoate (2.5-50 micrograms) plus 500 micrograms progesterone, all groups were inhibited by intraperitoneal (i.p.) treatment with 0.15 mg/kg 8-OH-DPAT. However, in the second week of hormone treatment, the effects of 8-OH-DPAT on lordosis behavior were dose-dependently attenuated by estradiol benzoate. Such attenuation was present when animals were treated with estradiol benzoate on the day of ovariectomy and when the first estradiol benzoate treatment was delayed for 2 weeks after ovariectomy. At least 3 days after the first injection with estradiol benzoate were required before the inhibitory effects of i.p. treatment with 8-OH-DPAT were attenuated. Although the magnitude was reduced, higher doses of 8-OH-DPAT (0.4, 0.45, and 0.5 mg/kg) continued to inhibit lordosis behavior even after the second hormonal priming. When 8-OH-DPAT was infused directly into the ventromedial nucleus of the hypothalamus (VMN), the lordosis-inhibiting effects of 8-OH-DPAT were reduced as soon as 2 days after the first estradiol benzoate injection. These data are interpreted as evidence that (1) estradiol benzoate's attenuation of the effects of 8-OH-DPAT on lordosis behavior is both dose and time dependent; (2) 5-HT1A receptor action in the VMN is attenuated by the hormone treatment; and (3) female gonadal hormones reduce the potency of the 5-HT1A agonist, 8-OH-DPAT, in inhibiting lordosis behavior.

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

A potential role of cyclic GMP in the regulation of lordosis behavior of female rats.

Nitric oxide (NO) has been suggested to play a crucial role in the regulation of lordosis behavior via stimulation of guanylyl cyclase to synthesize cyclic GMP. Whalen and Lauber (1986, Neurosci. Biobehav. Rev. 10, 47-53) hypothesized that hormones and pharmacological agents known to facilitate lordosis in estrogen-primed rodents act through cyclic GMP. The compound 1H-[1,2, 4]oxadiazolo[4,3-a]quinoxalin-1-one (ODQ) has been shown to selectively inhibit NO-stimulated cyclic GMP production. In the present study, we investigated the effects of ODQ on lordosis behavior. Female rats were implanted with a guide cannula aimed at the lateral or third ventricles by stereotaxic surgery, and their ovaries were bilaterally removed. Five days later, animals were injected subcutaneously with 2 microg estradiol benzoate at 48 and 24 hr, and 200 microg progesterone 4 hr before behavioral testing. ODQ or vehicle (1 microl) was administered at the time of progesterone treatment or 20 min before lordosis testing. ODQ significantly decreased lordosis quotients and the quality of lordosis at both intervals of drug infusion. Locomotor activities, measured by line crossing and rearing, were not affected by ODQ. ODQ also inhibited cyclic GMP accumulation in response to NMDA stimulation in hypothalamic and cerebellar slices in vitro. We conclude that cyclic GMP produced by NO generation is an important modulator of female rat sexual behavior.

Animals↗

Effects of pregnancy hormones on maternal responsiveness, responsiveness to estrogen stimulation of maternal behavior, and the lordosis response to estrogen stimulation.

The aim of the study was to determine whether there is an increase in responsiveness to estrogen stimulation of maternal behavior and lordosis responsiveness during pregnancy. Using separate groups of pregnancy-terminated females, we measured the initial maternal responsiveness of hysterectomized-ovariectomized (HO) females and their responsiveness to estrogen stimulation. Maternal behavior latencies were studied in females HO on the 8th, 10th, 13th, 16th, or 19th day of pregnancy (8HO-19HO) and in nonpregnant HO (NPHO) females. Groups were injected sc with estradiol benzoate (EB) in doses ranging from 0 to 200 microgram(s)/kg and tested for maternal behavior (retrieving, crouching, and licking pups). In addition, we investigated whether there is an increase during pregnancy (following HO) in lordosis responsiveness to estrogen stimulation. Lordosis behavior was studied in pregnant HO females (days 8, 16, and 22) and NPHO females given 0 to 200 microgram(s)/kg EB. There was an increase in maternal responsiveness in oil-treated HO females starting around midpregnancy. From early pregnancy on there was also an increase in maternal responsiveness to 20 microgram(s)/kg EB. In late pregnant females (16HO) there was a further increase with 50 microgram(s)/kg EB. There was no increase in lordosis responsiveness to EB stimulation during pregnancy; pregnant and nonpregnant HO females had the same EB threshold for stimulating lordosis behavior. The results of both studies were related to increases during the latter half of pregnancy in nuclear estrogen receptor concentrations in the MPOA, an area that mediates estrogen stimulation of maternal behavior, and the absence of such increases during pregnancy in the VMH, an area that mediates estrogen stimulation of lordosis behavior.

Animals↗

Inhibition of lordosis behavior in male and female rats by androgens and progesterone.

Several studies suggest that when manipulated experimentally in adulthood, the lordosis response to estrogen can be increased dramatically in male rats. Because adult-gonadectomized (Gx) animals were used in these studies, the lack of testicular hormones in adulthood may have been a factor. To examine this possibility, adult-Gx rats were implanted with blank (Bk)-, testosterone (T)-, 5alpha-dihydrotestosterone (DHT)-, or progesterone (P)-filled capsules, alone or in combination. We report a new finding, that a combined treatment of T plus P (T+P) at physiological doses for the male, but not T or P alone, reduced lordosis significantly in males, with and without estrogen priming. T+P did not inhibit lordosis in females, nor did this specific treatment affect open field, aggressive, and male copulatory behaviors. In confirming studies done with much higher doses, DHT reduced lordosis in both sexes. DHT and T+P also reduced lordosis in adrenalectomized/Gx males. Mechanisms responsible for the T+P inhibition of lordosis in males are not known, but they may include an upregulation of androgen receptors by P, and this possibility is discussed.

Adrenalectomy↗

Influence of gamma-aminobutyric acid on lordosis behavior and dopamine activity in estrogen primed spayed female rats.

In the first experiment the role of gamma-aminobutyric acid (GABA) in the display of lordosis behavior was examined in septal-lesioned and sham-operated ovariectomized rats. Following estradiol benzoate (EB) priming, septal-lesioned rats were tested for lordosis behavior before and after bilateral infusion of picrotoxin or saline directly into the substantia nigra (SN). Sham animals were given the same behavioral tests but received intranigral infusion of either hydrazinopropionic acid (HPA) or saline. Picrotoxin, which blocks GABA receptors, was effective in suppressing the high levels of lordosis behavior seen in the EB-primed septal-lesioned female rat 30 min after infusion, but not at 120 min. Conversely, HPA, which elevates endogenous GABA levels, was effective in facilitating lordosis behavior in sham-operated rats treated with EB only. The lordosis quotient was moderately increased 30 min after HPA infusion, reached high levels at 120 min, and returned to low levels by 360 min post-infusion, demonstating the reversibility of the drug effect. Saline infusions in lesioned and sham-operated controls were without effect. In the second experiment sepal-lesioned and sham-operated rats were primed with EB and infused with the drugs as in the first experiment, but were sacrificed at the time the macimal behavioral effect had been observed in the first experiment. Tyrosine hydroxylase (TH) activity and dopamine (DA) and homovanillic acid (HVA) levels were measured. No effect on TH activity was found. However, sham-operated rats receiving HPA infusions had lower DA and HVA levels compared to those of saline-injected controls, and septal-lesioned rats receiving picrotoxin infusions had higher DA and HVA levels than those of lesioned saline-injected controls. Septal-lesioned saline-infused rats also showed decreased DA and HVA levels relative to sham-operated saline-infused animals. These results support the concept of a GABA inhibitory neuronal feedback system which modulates DA turnover and perhaps plays a critical role in the neural control of lordosis behavior.

Animals↗

Alpha 1-noradrenergic regulation of hypothalamic progestin receptors and guinea pig lordosis behavior.

Experiments were conducted to determine whether alpha 1- or alpha 2-receptors mediate noradrenergic (NA) regulation of guinea pig lordosis behavior and hypothalamic progestin receptors. When infused into a lateral cerebroventricle at a dose that inhibits lordosis and that decreases the concentration of estradiol-inducible hypothalamic progestin receptors, phenoxybenzamine decreased binding of the alpha 1-ligand [3H]WB4101 but not the alpha 2-ligand [3H]clonidine to brain membranes. Thus, under the conditions used, phenoxybenzamine appears to block alpha 1-receptors with little or no effect on alpha 2-receptors. Experiments with the selective alpha 1-antagonist prazosin also indicated alpha 1-receptor regulation of lordosis and hypothalamic progestin receptors. Prazosin inhibited lordosis induced by estradiol benzoate (EB) plus progesterone and by EB + clonidine and decreased the concentration of cytoplasmic progestin receptors in hypothalamus (but not in preoptic area or frontal cortex) of EB-primed females. The inhibition of lordosis is apparently not due to some unknown side effect of prazosin because pretreatment with a high dose of clonidine attenuated the inhibition. The possibility that a causal relationship exists between effects of alpha 1-NA transmission on hypothalamic progestin receptors and lordosis was discussed. Also, because effects of NA transmission on hypothalamic progestin receptors are dependent on prior treatment with EB, it was suggested that NA transmission might influence estradiol action in addition to progestin action in hypothalamic cells.

Animals↗

Ibotenic acid-induced lesions of the medial preoptic area/anterior hypothalamus enhance the display of progesterone-facilitated lordosis in male rats.

Electrical lesions of the medial preoptic area/anterior hypothalamus (MPOA/AH) have been reported to enhance the display of steroid-induced lordosis in castrated male rats. This study employed the cell body-specific neurotoxin, ibotenic acid, to ascertain whether neurons originating in this region (as opposed to axons of passage) tonically inhibit steroid-induced lordosis in adult male rats. Castrated, adult Long-Evans males received bilateral electrical lesions or injections of ibotenic acid or vehicle aimed at the MPOA/AH. Following administration of estradiol benzoate (EB) and progesterone, lordosis quotients (LQs) and lordosis ratings (LRs) were significantly higher in groups of rats with electrical lesions (LQ = 62.2 +/- 15.1; LR = 1.22 +/- 0.34) and ibotenic acid-induced lesions (LQ = 58.1 +/- 12.2; LR = 0.99 +/- 0.24) than in the control group (LQ = 12.8 +/- 7.3; LR = 0.22 +/- 0.13). To determine whether this enhancement of receptive behavior in MPOA/AH-lesioned males was an effect on estradiol-induced, as compared to progesterone-facilitated lordosis, groups of castrated rats in a second experiment received bilateral injections of ibotenic acid or vehicle aimed at the MPOA/AH and were tested for lordosis after administration of EB alone and again after injection of progesterone. Following treatment with EB alone, rats with ibotenic acid-induced MPOA/AH lesions tended to be slightly less receptive than control animals. However, following injections of progesterone, LQs and LRs were higher in the MPOA/AH-lesioned group than in the control animals, as had been observed in the first experiment.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

The role of the medial nucleus of amygdala in the mating-induced enhancement of lordosis in female rats: the interaction with luteinizing hormone-releasing hormone neuronal system.

The effect of bilateral lesion of the medial nucleus of amygdala (mAMY) on the mating-induced enhancement of lordosis behavior in ovariectomized (OVX) estrogen-primed rats was investigated. The enhancement of lordosis following repeated coital stimulation was significantly reduced in the mAMY-lesioned rats as compared with the sham-operated controls. Double labeling immunocytochemistry of the brain of the repeatedly mated females for Fos protein and luteinizing hormone-releasing hormone (LHRH) revealed that a significantly lower percentage of the LHRH neurons in the mAMY-lesioned females exhibited Fos immunoreactivity than the controls. This suggests that bilateral destruction of the mAMY suppresses the activation of the LHRH neuronal system following repeated mating. Furthermore, the correlation between the number of Fos-positive LHRH neurons and lordosis-to-mount ratio in the sham-females was significant, while a similar comparison in mAMY-lesioned females was not significant. Since LHRH is reported to enhance lordosis behavior in OVX estrogen-primed rats, it appears likely that the effects of mAMY on lordosis are mediated through the LHRH neuronal system. The results further support the involvement of the accessory olfactory system in the mating-induced enhancement of lordosis behavior in female rats.

Amygdala↗

Effects of voluntary and forced exercise on lordosis behavior in female rats.

We measured sexual behavior (lordosis) in ovariectomized, steroid-treated, exercising female rats. When estradiol-treated animals exercised voluntarily, lordosis was directly related to the amount of exercise. Forced exercise (swimming) following treatment with estradiol 17 beta and progesterone significantly increased lordosis scores but only after animals swam for 2.5 hr per day. Lordosis behavior returned to baseline levels 7 weeks after forced exercise was stopped. Circulating levels of estrogen and progesterone measured immediately after behavioral testing did not differ between animals forced to exercise and their controls. The mechanisms responsible for the increase in lordosis behavior following exercise are unclear. It is possible that a change in body composition, a change in neural sensitivity to gonadal steroids, and/or changes in pituitary or adrenal function contribute to the increased lordosis behavior in exercised animals.

Animals↗

Facilitation of lordosis in guinea pigs by an alpha-noradrenergic agonist is independent of progestin receptor stimulation.

Because manipulations of the noradrenergic system affect both lordosis behavior and progestin receptor levels in female guinea pigs, the present study attempted to determine if the noradrenergic (NE) system affects lordosis solely because of its impact on progestin receptors. Although the progestin receptor antagonist RU486 significantly reduced progesterone-facilitated lordosis, it had no effect on lordosis induced by the alpha-NE agonist clonidine in estrogen-primed female guinea pigs. This indicates that although progesterone may facilitate lordosis in female guinea pigs via activation of progestin receptors, the alpha-noradrenergic agonist clonidine does not mediate lordosis through the same mechanism.

Animals↗

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).

Afferent Pathways↗

Inhibition of guinea pig lordosis behavior by the phenylethanolamine N-methyltransferase (PNMT) inhibitor SKF-64139: mediation by alpha noradrenergic receptors.

Experiments were undertaken to determine whether the steroid-dependent lordosis response of female guinea pigs is under adrenergic control. In initial experiments, treatment with the centrally active phenylethanolomine N-methyltransferase (PNMT; the enzyme catalyzing methylation of norepinephrine to epinephrine) inhibitor SKF-64139 inhibited lordosis behavior induced by estradiol-17 beta benzoate plus progesterone. SKF-29661, a PNMT inhibitor that does not cross the blood-brain barrier, did not affect lordosis. However, no detectable epinephrine was found in brain or spinal cord of drug- or vehicle-treated guinea pigs. This suggests that epinephrine neuronal systems do not exist in the guinea pig CNS. In agreement with this idea, the inhibitory effects of SKF-64139 on lordosis were found to be primarily attributable to the blockade of alpha noradrenergic receptors rather than to PNMT inhibition. Two lines of evidence support this conclusion. First, using in vitro receptor binding techniques, SKF-64139 was found to have a relatively high affinity for alpha 1 and particularly alpha 2 receptors in guinea pig forebrain. Second, presumably through competitive inhibition of SKF-64139 binding to alpha receptors, treatment with clonidine (an alpha receptor agonist) overrode the inhibitory effects of SKF-64139 on lordosis. Taken together, these findings indicate the possible absence of epinephrine neuronal systems in guinea pig brain and reemphasize the importance of alpha receptors in regulating steroid-dependent lordosis behavior in this species.

Animals↗

Lordosis behavior in intact male rats: effects of hormonal treatment and/or manipulation of the olfactory system.

The aim of this study was to investigate the olfactory mechanisms regulating the display of lordosis behavior in intact Wistar male rats bred in our colony. Gonadally intact males show a low capacity to respond by lordosis to male mounts and were insensitive to manipulations of the olfactory system (exposure to the odor of male urine or accessory bulb removal (AOBR)) which have been previously shown to facilitate the display of lordosis behavior in orchidectomized animals primed with ovarian hormones. Treatment with either estradiol benzoate (EB) or EB and progesterone (P) consecutively did not render these gonadally intact animals sensitive to the effects of AOBR. By contrast exposure to male urine was capable of facilitating the display of lordosis behavior in intact male rats given EB + P consecutively. These results are discussed in the light of previous findings showing that (1) two inhibitory structures, the accessory olfactory bulb and the septal and preoptic areas, are involved in the control of lordosis behavior in the male rat; (2) the effects of olfactory cues on the display of lordosis behavior are dependent on the action of both EB and P in orchidectomized animals.

Animals↗

Inhibitory effects of the 5-HT1A agonists, 5-hydroxy- and 5-methoxy-(3-di-n-propylamino)chroman, on female lordosis behavior.

Sexually receptive, intact, proestrous rats were infused bilaterally into the ventromedial nucleus of the hypothalamus with one of several serotonin (5-HT) agonists and with the endogenous ligand, 5-HT. Serotonin (2000 ng) and the 5-HT1A agonists, 8-hydroxy-2-(di-n-propylamino)tetralin [8-OH-DPAT (200 ng)], 5-methoxy-3-(di-n-propylamino)chroman [5-MEO-DPAC (200-2000 ng)] and 5-hydroxy-3-(N-di-n-propylamino)chroman [5-OH-DPAC (200-2000 ng)] inhibited female lordosis behavior within 10 min of the infusion. The rank order of the effectiveness of these compounds was 8-OH-DPAT > 5-OH-DPAC > or = 5-MEO-DPAC > 5-HT. The nonselective 5-HT agonist, 1-(m-trifluoromethyl) piperazine [TFMPP (2000 ng)], did not reduce lordosis behavior. In addition to their reduction of lordosis behavior, the 5-HT1A agonists elicited resistive behavior toward the male's attempts to mount. There were minimal effects of the 5-HT1A agonists on either quality of the lordosis reflex or on proceptivity. However, rats pretreated with TFMPP and infused with 8-OH-DPAT 1 hr later, did show a transient suppression of lordosis quality. These results provide further evidence that the ventromedial nucleus of the hypothalamus contains 5-HT1A sites, the activation of which reduces lordosis behavior in regularly cycling, proestrous rats.

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