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PubMed1998

Sexual behavior of Flinders Line female rats bred for differential cholinergic sensitivities.

Flinders Lines are two strains of rats selectively bred for their divergent physiological responses to cholinergic drug challenges. Flinders Sensitive Line (FSL) rats are highly sensitive to cholinergic stimulation of various autonomic and behavioral responses compared to Flinders Resistant Line (FRL) rats. Because cholinergic innervation contributes to the regulation of female sexual behaviors in rats, a study was conducted to compare the sexual responses of FSL females to those of FRL females, as well as to those of Long-Evans (LE) females, a conventional rat strain. Ovariectomized FSL rats exhibited significantly higher incidences of lordosis and proceptive behaviors than ovariectomized FRL and LE rats over a range of estrogen doses (2, 3, 4, 5, or 20 microgram(s)/kg estradiol benzoate at 48 h before testing) administered in combination with progesterone (1 or 2 mg/kg at 4-6 h before testing). In addition, the muscarinic antagonist scopolamine inhibited lordosis behavior strongly in FRL females over a range of doses (0.25, 0.5, 1, 2, or 4 mg/kg), but failed to inhibit lordosis in FSL females. Results indicate that FSL females are highly sensitive to the behavioral effects of gonadal steroids and highly insensitive to the effects of a muscarinic antagonist. The enhanced sexual behavioral responses of FSL females could be a consequence of their well-established cholinergic hypersensitivity or a consequence of other undocumented characteristics of FSL females such as hypersensitivity to ovarian hormones. FSL females could provide a valuable model for the study of estrogen action at behavioral, cellular, and molecular levels.

Animals↗
PubMed2000

Appetitive and consummatory sexual behaviors of female rats in bilevel chambers. II. Patterns of estrus termination following vaginocervical stimulation.

Copulation with intromission or manual vaginocervical stimulation (VCS) shortens the duration that intact female rats maintain lordosis responding during estrus. The present study examined whether VCS could shorten the duration of both appetitive and consummatory measures of female sexual behavior, and whether these effects occur differentially in time and across different hormone priming intervals. Ovariectomized, sexually experienced female rats were administered subcutaneous injections of estradiol benzoate 48 h and progesterone 4 h, before receiving 50 manual VCSs with a lubricated glass rod distributed over 1 h. Control females received sham VCSs distributed over the same time. The females were then tested for sexual behavior in bilevel chambers with two sexually vigorous males (to one ejaculatory series or 10 min with each male, separated by 5 min) 12, 16, and 20 h after VCS. Prior to the final hormone treatment, different groups of females had been given the same hormone treatment either 28, 14, 7, or 4 days before. In females tested at 28- and 14-day hormone intervals, VCS induced both active and passive rejection responses at 12, 16, and 20 h. In contrast, females that received sham VCS displayed relatively normal sexual behavior at 12 h, although by 16 and 20 h these females displayed active and passive rejection. Females tested at 7- or 4-day intervals displayed normal levels of lordosis at all testing times, regardless of VCS treatment. These data indicate that VCS facilitates rejection responses that precede the decrease in lordosis responsiveness. However, the effects of VCS are dependent on the frequency of hormone priming, suggesting that hormone treatment may block some of the long-term inhibitory effects of VCS on female sexual behavior.

Animals↗
PubMed2001

The synaptic organization of VMH neurons that mediate the effects of estrogen on sexual behavior.

Estrogen acts in the hypothalamic ventromedial nucleus (VMH) of female rats to promote sexual behavior, as typified by the lordosis response. Morphological changes in the VMH, such as increased synaptic profiles and increased dendritic spines, suggest that estrogen may modulate behavior by altering VMH synaptic organization. To understand the significance of these changes, this laboratory has been investigating the functional classes of lordosis-relevant neurons and their local connectivity. A neurotropic virus, pseudorabies virus (PRV), was used to transneuronally label the CNS network that controls the lordosis-producing muscles. When PRV was placed in the lumbar epaxial muscles, it was sequentially detected in the lumbar ventral horn, the medullary reticular formation, the periaqueductal gray, and finally the VMH. Subsequent analysis showed that the population of VMH neurons that were initially infected with PRV largely resided beyond the cluster of estrogen receptor-containing neurons. In a separate study, VMH neurons were visualized with Lucifer yellow, and their morphology was analyzed using confocal microscopy. Such analysis confirmed that estrogen treatment increased dendritic spines in the VMH. The particular VMH neurons in this study did not express nuclear estrogen receptor, which suggests that estrogen can increase spine density indirectly. These results represent initial steps toward unraveling the local circuit that mediates estrogenic action on a specific reproductive behavior.

Animals↗
PubMed1988

Estrogen-induced alterations in synaptic morphology in the midbrain central gray.

Axons of ventromedial hypothalamic (VMH) neurons have been previously shown to terminate in the midbrain central gray (MCG) (Chung et al. 1984, 1986). Since VMH synapses in this region may be involved in the mediation of estrogen-induced lordosis behavior, we examined the effect of estrogen on the morphology of synapses in the MCG. Ovariectomized adult female rats were given daily subcutaneous injections of estradiol benzoate (10 micrograms) or the vehicle control and after 20 days of injection, only the estrogen-treated rats showed the lordosis response. A quantitative analysis of MCG tissue from these animals demonstrates morphological changes in various synaptic parameters with estrogen treatment including: 1) an increase in the mean number of dense-cored vesicles and an increase in the number of terminals containing dense-cored vesicles, 2) an increase in the length of postsynaptic densities (PSDs), 3) an increase in the number of PSDs showing perforations, 4) an increase in the number of synapses, and 5) an increase in the number of synapses with positive synaptic curvature. No alterations in the number of subjunctional bodies were observed. The dense-cored vesicles may contain an estrogen-induced trophic factor which may function in maintaining the integrity of postsynaptic processes and cells in the MCG with which VMN endings contact (Chung et al. submitted) and/or which induces morphological changes in postsynaptic structures which facilitate the effects of estrogen on lordosis behavior.

Animals↗
PubMed1996

Lordotic alignment and posterior migration of the spinal cord following en bloc open-door laminoplasty for cervical myelopathy: a magnetic resonance imaging study.

We investigated lordotic alignment and posterior migration of the spinal cord following en bloc open-door laminoplasty for cervical myelopathy. Fifty-five patients (32 men and 23 women) were studied, with an average follow-up of 2.4 years. Radiological examination included evaluation of lordosis of the cervical spine and spinal cord, degree of enlargement of bony spinal canal, and the magnitude of posterior cord migration. We also correlated these changes with neurological improvement. Postoperatively, there was an average of 5% loss of cervical spine lordosis (P > 0.01) on radiographs and 12% reduction in the lordotic alignment of the spinal cord (P > 0.05) on magnetic resonance imaging. Postoperatively, the size of the bony spinal canal increased by 48%. Posterior cord migration showed a significant correlation with the preoperative cervical spine and spinal cord lordosis (P < 0.05). Thirty-seven (67%) patients with neurological improvement exceeding 50% showed significant posterior cord migration following laminoplasty compared with those demonstrating less than 50% improvement (P = 0.01). Our results suggest that a significant neurological improvement is associated with posterior cord migration after cervical laminoplasty.

Adult↗
PubMed2004

In the ventral tegmental area picrotoxin blocks FGIN 1-27-induced increases in sexual behavior of rats and hamsters.

RATIONALE AND OBJECTIVES: There are two types of benzodiazepine receptors, mitochondrial benzodiazepine receptors (MBRs), and gamma-aminobutyric acid (GABA(A))/benzodiazepine receptor complexes (GBRs). MBR activation increases neurosteroidogenesis. Ventral tegmental area (VTA) infusions of the MBR agonist, FGIN 1-27, increase midbrain levels of the progesterone metabolite 5alpha-pregnan-3alpha-ol-20-one (3alpha,5alpha-THP) and lordosis of rats and hamsters. Activation of GBRs leads to membrane hyperpolarization. In the VTA, infusions of GBR agonists enhance 3alpha,5alpha-THP-facilitated lordosis. Thus, if, in the VTA, MBR-mediated increases in 3alpha,5alpha-THP enhance sexual responses via actions at GBRs, then blocking GBRs with picrotoxin will reduce FGIN 1-27-induced increases in sexual behavior of female rodents. METHODS: Ovariectomized rats and hamsters, with unilateral guide cannula to the VTA, received estradiol benzoate (10 mug; EB) at hour 0. Hamsters also received progesterone (100 mug) at hour 44. At hour 47.5, all animals were infused first with 10 ng or 20 ng picrotoxin or saline, vehicle to the VTA and, 30 min later, with 5 mug/11.4 nM FGIN 1-27 or saline, vehicle. Ten minutes later, animals were tested for sex and motor behavior. RESULTS: Picrotoxin, but not vehicle, infusions blocked FGIN 1-27-mediated increases in lordosis of rats and hamsters, proceptivity of rats, and sexual responsiveness of hamsters. In addition, midbrain 3alpha,5alpha-THP levels were higher in animals that received VTA infusions of FGIN 1-27, compared to those infused with saline, vehicle. CONCLUSION: In the VTA, GBRs are required for MBR-enhanced sexual behavior of EB-primed rats and EB- and progesterone-primed hamsters.

Animals↗
PubMed2002

Burst fracture of the fifth lumbar vertebra: results of posterior internal fixation and transpedicular bone grafting.

Burst fractures of the fifth lumbar vertebra are rare, and there are only a few reports on this subject, which is characterised by its unique anatomical and biomechanical features. This retrospective analysis reports on ten patients whose fractures of L5 were stabilised with a short internal fixator in combination with a posterior fusion as well as transpedicular bone grafting. The average follow-up period was 22 months. Radiometric data were surveyed and compared to the functional results. The height of the fractured vertebra remained nearly unchanged throughout the course. Loss of lordosis of 4 degrees in the upper disc space and 4 degrees in the lower disc space were observed postoperatively. At the time of follow-up, the values of segmental lumbar lordosis were significantly below the preoperative level. The narrowing of the neural canal was reduced from 57% to 28% with the surgical intervention. However, there was no correlation between the functional and the radiological outcome. Neurological deficits were documented in two patients, which declined during the course. There were no severe postoperative complications. The results of the present study demonstrate that the described surgical procedure in fractures of the fifth lumbar vertebra does not promote an anatomic restoration of the fractured vertebra, nor of the segmental lordosis. However, the clinical results do not correlate with the radiological outcome. Nonoperative treatment with early mobilisation without external support seems to be the treatment of choice.

Adolescent↗
PubMed1998

Simultaneous combined anterior and posterior lumbar fusion with femoral cortical allograft.

The radiographic fusion rates, graft behaviour and clinical outcome of 41 patient with simultaneous combined anterior lumbar interbody fusion and posterior arthrodesis with translaminar screws were reviewed independently. In all patients a femoral cortical allograft (FCA) ring filled with autologous iliac crest cancellous bone was used anteriorly to replace the disc and achieve interbody fusion. The follow-up averaged 30.6 months, with a minimum follow-up of 24 months. All patients had disabling low-back pain with different degrees of radiating leg pain and either discogenic pain (n = 24) or a postdiscectomy syndrome (n = 15) respectively postfusion syndrome (n = 2). The overall fusion rate was 95.2% (59 of 62 segments). Time to radiographic fusion averaged 8.7 months (range 2-34 months), and in 66.1% radiographic fusion occurred without significant subsidence. In 18.6% fusion with subsidence resulted from resorption of the FCA and in 15.3% the FCA had protruded into the vertebral body. The posterior intervertebral disc height (PIVDH) increased postoperatively by 2 mm on average. However, loss of PIVDH was the rule, and occurred within the first 12 postoperative months, resulting in a negligible final gain in height of 0.3 mm on average. The segmental lordosis was increased by 3 degrees; however, loss of lordosis during the first 6 postoperative months led to a final gain in lordosis of 1.3 degrees on average. Graft incorporation occurred in 16 of 62 segments (25.8%) and was observed at an average of 21.9 months postoperatively. Subjectively, 82.4% of the patients were satisfied or highly satisfied with the clinical result of the fusion operation. In conclusion, the described technique has proven to be highly effective in achieving a high fusion rate with a good patient outcome.

Adult↗
PubMed1978

Selective enhancement of the lordotic component of female sexual behavior in rats following destruction of central catecholamine-containing systems.

Ovariectomized female rats received two intraventricular injections of 200 microgram of 6-hydroxydopamine (6-OHDA), a treatment which produced 66% depletion of telencephalic norepinephrine and 53% depletion of telencephalic dopamine. Compared to vehicle-injected controls, 6-OHDA-treated animals showed increased lordosis scores when treated with ovarian hormones. This effect was potentiated by additional treatment with 100 mg/kg alpha-methyl-p-tyrosine (AMT), a catecholamine synthesis inhibitor. Besides showing increased frequency and intensity of lordosis, animals treated with both 6-OHDA and AMT retained the lordotic posture significantly longer after the male dismounted than animals given either treatment alone or vehicle controls. The enhancement of lordosis following CA depletion was not prevented by a series of dexamethasone treatments which caused a marked suppression in adrenal steroid (corticosterone) levels. This suggests that normal adrenal function is not a prerequisite for the observed enhancements. It was concluded that the lordotic response is inhibited by the activity of a catecholamine system. Soliciting behavior (hop-darting) was not enhanced by any treatment, suggesting that catecholamine activity has an inhibitory influence on the stop component of sexual behavior, but not on the whole copulatory pattern.

Animals↗
PubMed1988

Bethanechol-induced increase in hypothalamic estrogen receptor binding in female rats is related to capacity for estrogen-dependent reproductive behavior.

Neuroactive agents associated with different neurotransmitter systems can modulate the number of hypothalamic estrogen binding sites. It has been demonstrated previously that the muscarinic cholinergic agonist, bethanechol, administered 30 min prior to in vitro estrogen receptor assays increases the concentration of hypothalamic estrogen binding sites by 30-35% in female rats. Bethanechol was without effect on male hypothalamic preparations. In order to investigate further this sex difference and in an attempt to determine a relationship between the modulation of estrogen binding sites and a sexually differentiated function, bethanechol was given to female rats rendered either anovulatory and capable of displaying lordosis or anovulatory and behaviorally insensitive to estrogen. The results showed that bethanechol significantly increased the number of estrogen binding sites in females capable of displaying lordosis but not in females which did not show this estrogen-dependent behavior. It is possible that the capacity for drug-induced modulation of estrogen binding sites could be related functionally to the ability to display lordosis behavior.

Animals↗
PubMed1988

Steroids induce hypothalamic progestin receptors and facilitate female sexual behavior in neonatal rats.

This report provides the first evidence that two activational actions of estrogen can occur within the first week of life in the rat. Priming 4-day-old rats with exogenous estradiol benzoate facilitates lordosis and ear wiggling-like behavior, and induces cytosol progestin receptors in the medial basal hypothalamus and preoptic region (Hyp-PoA) 44 h later. Moreover, unprimed male infants show more intense lordosis and higher concentrations of cytosol progestin receptors in Hyp-PoA than infant females. Neonatal castration of male infants decreases their concentration of cytosol progestin receptors in Hyp-PoA to the levels normally seen in infant females. In addition, priming 6-day-old infants with progesterone alone facilitates lordosis in male but not female infants. Together, these data demonstrate that in the male infant, endogenous steroids of testicular origin have activational as well as organizational actions.

Animals↗
PubMed1990

Differential regulation of proenkephalin gene expression by estrogen in the ventromedial hypothalamus of male and female rats: implications for the molecular basis of a sexually differentiated behavior.

The ventrolateral aspect of the ventromedial hypothalamic nucleus (VL-VM) contains many estrogen-concentrating neurons which mediate estrogen facilitation of reproductive behavior. Previous studies have shown that estrogen treatment increases proenkephalin (PE) gene expression in neurons of the VL-VM in ovariectomized female rats, and that enkephalin peptides may stimulate lordosis behavior. To determine whether there is a sex difference in steroid hormone regulation of PE gene expression we have examined the effects of estrogen and testosterone on PE mRNA levels in male rats. Slot blot hybridization analysis of RNA isolated from the ventromedial hypothalamus indicated that estrogen treatment increased PE mRNA levels in the VL-VM of ovariectomized female rats (2.2-fold), but had no measurable effect on PE mRNA levels in gonadectomized males. Testosterone treatment of gonadectomized males also had no effect on PE gene expression. To determine whether the sex difference in estrogen-inducibility of PE gene expression is due to the developmental effects of gonadal steroids, we have investigated the effect of estrogen on PE mRNA levels in the VL-VM of neonatally androgenized female rats. Unlike the genetic male, the androgenized females responded to estrogen treatment with a female-typical increase in PE mRNA levels (1.7-fold). Further, although the androgenized rats clearly exhibited signs of defeminization, they did exhibit estrogen-facilitated lordosis behavior when tested with manual stimulation. The PE mRNA induction in estrogen-treated androgenized rats correlated well with the lordosis scores obtained by manual stimulation testing. These results indicate that estrogen regulation of PE gene expression in the VL-VM is sexually differentiated and support the hypothesis that the enkephalinergic neurons of the VL-VM are involved in the regulation of female reproductive behavior.

Animals↗
PubMed1990

Progestin receptors in the ventromedial nucleus of the hypothalamus and arcuate nucleus-median eminence are decreased by idazoxan.

Steroid-dependent lordosis behavior in ovariectomized (OVX) guinea pigs is attenuated by alpha 1- and/or alpha 2-noradrenergic (NE) receptor antagonists. Correlated with the decrease in lordosis after alpha 1-NE receptor blockade by prazosin is a decrease in 'cytosol' progestin receptors in the ventromedial hypothalamic nucleus (VMN). We examined whether a presumed alpha 2-NE receptor blocker (idazoxan, IDA) also affects progestin receptors. A decrease in 'cytosol' progestin receptors was found after IDA treatment of OVX, estrogen-treated guinea pigs in the VMN and the arcuate nucleus-median eminence (ARC-ME). Apparently, either prazosin or IDA can inhibit lordosis behavior and decrease 'cytosol' progestin receptors in the VMN. In contrast, idazoxan but not prazosin, decrease 'cytosol' progestin receptors in the ARC-ME.

Adrenergic alpha-Antagonists↗
PubMed1985

Duration of hormonal deprivation: influences on physiological and behavioral responsiveness to estradiol.

A total of 54 ovariectomized female guinea pigs were divided into three groups and tested six times at 2-week intervals for their responsiveness to exogenous ovarian hormones (3 days of 4 micrograms/kg estradiol benzoate plus 1 day of 0.4 mg/kg progesterone) or control injections (0.2 ml oil vehicle). Two weeks after ovariectomy, treatment with estradiol significantly reduced food intake and body weight, and also produced vaginal membrane rupture in 98.1% of the females. When tested for sexual behavior at 4, 6, and 8 hr after the progesterone injection, 29 of the subjects (53.7%) displayed lordosis in response to manual stimulation. Twelve weeks after ovariectomy, the effects of estradiol on food intake, body weight, and vaginal membrane condition had not diminished. However, the overall proportion of females from which lordosis could be elicited declined to 27.8%. Biweekly injections of estradiol benzoate plus progesterone to one of the groups of females did not prevent this decline in the sexual response. Based on these results, it was concluded that the observed reduction in behavioral lordosis does not represent a general decline in the responsiveness of ovariectomized guinea pigs to estrogenic stimulation, but may involve changes in their responsiveness to progesterone or in other mechanisms more specifically associated with sexual behavior.

Animals↗
PubMed1985

Specificity and neural sites of action of anisomycin in the reduction or facilitation of female sexual behavior in rats.

These experiments were designed to investigate the role of neuronal protein synthesis in the hormonal activation of female sexual behavior using intracranial implants of the protein synthesis inhibitor, anisomycin. In the first experiment, female rats receiving bilateral cannulae implants in the medial preoptic area (POA), septal region (SEPT), ventromedial hypothalamus (VMH), or midbrain central gray (CG) were injected with 2.5 micrograms estradiol benzoate (EB), followed 48 hr later by 500 micrograms progesterone (P). Females receiving anisomycin in the VMH at the time of EB injection had lower levels of lordosis and darting compared to tests without anisomycin. Sexual behavior was unaffected in females receiving anisomycin implants in the POA, SEPT, or CG. In a second experiment, we replicated the finding that anisomycin could attenuate lordotic responsivity when placed in the VMH of female rats injected with 2.5 micrograms EB and 500 micrograms P. In addition, we found that POA implants of anisomycin could facilitate lordosis in females given a low dose of EB (1.25 microgram) plus 500 micrograms P. In a third experiment, we assessed the effects of anisomycin application to the VMH or POA of female rats receiving estradiol (E; diluted 1:250 with cholesterol) implants in the VMH and systemic P. Treatment of the VMH with anisomycin prior to E in the VMH suppressed lordotic responding, whereas anisomycin application to the POA prior to E in the VMH had no effect on lordosis. The results of these experiments suggest that reducing protein synthesis in the region of the VMH disrupts the action of estrogen on the VMH, and that the facilitative action of anisomycin in the POA of female rats requires more estrogen treatment than threshold stimulation of the VMH alone.

Animals↗
PubMed1985

Estrogens before birth and development of sex-related reproductive traits in the female guinea pig.

Influences of estrogens on the differentiation of psychosexual traits in the female guinea pig were studied. Pregnant animals were injected intramuscularly with either 1, 2, or 3.3 micrograms estradiol benzoate (EB) or with 1 or 3 micrograms diethylstilbestrol dipropionate (DESDP). Injections were started on the 29th day of pregnancy, given daily for 6 days, and continued every other day until parturition. Female offspring were evaluated for onset of puberty, ovarian function, and lordosis and mounting behavior in adulthood. Prenatal treatment with 3 micrograms DESDP caused delayed puberty, impaired ovarian function, reduced responsiveness of lordosis to EB and P in adulthood (defeminization), augmented mounting in the absence of hormones (masculinization), and reduced responsiveness of mounting to exogenous EB and P in adulthood (defeminization). Prenatal treatment with 1 microgram DESDP produced similar but less pronounced effects. Prenatal treatment with 3.3 micrograms EB also caused a delay in puberty. However, responsiveness of lordosis to EB and P in adulthood was enhanced by treatment with either 1 or 3.3 micrograms EB prenatally. Further, neither mounting in the absence of hormones nor mounting in response to EB and P in adulthood were affected in any measurable way by any prenatal treatment with EB. These results show that estrogens can have masculinizing and defeminizing effects on sexually dimorphic reproductive traits in guinea pigs. The failure of EB to duplicate or parallel the effects of DESDP is not completely understood at this time, but it may indicate that less of the active substance reaches the target tissues following maternal and placental metabolism of EB than of DESDP.

Animals↗
PubMed1990

Facilitation of sexual receptivity in hamsters by simultaneous progesterone implants into the VMH and ventral mesencephalon.

Intracranial implantation experiments have shown that the ventromedial hypothalamus (VMH) is the most sensitive site for the facilitation of female sexual behavior by progesterone in estrogen-primed rats. However, similar implantation techniques have been much less successful in hamsters. Several lines of evidence indicate that both hypothalamic and midbrain structures are important for hamster lordosis. Therefore we compared the effect of progesterone (P) implants administered simultaneously to VMH and ventral midbrain on opposite sides of the brain to the effects of bilateral implants to each of these sites separately. Ovariectomized female hamsters were stereotaxically implanted with 24-gauge thin-wall guide tubes according to one of five patterns. Bilaterally symmetrical cannulae were aimed at VMH or ventral mesencephalon (vMES) or asymmetrical implants were aimed at one of the following pairs of sites, on opposite sides of the brain: VMH-vMES, VMH-preoptic area (VMH-POA), or anterior hypothalamus-anterior mesencephalon (AH-aMES). After recovery from surgery, females were primed with 10 micrograms estradiol benzoate and given pellets of P or cholesterol through a 30-gauge injector in the targeted sites. Latency, frequency, and duration of lordosis were recorded in 10-min tests with sexually active male hamsters. Sexual receptivity was significantly facilitated by simultaneous contralateral P implants into the VMH-vMES. P implants in any other combination of sites did not significantly facilitate lordosis compared to cholesterol control implants, nor did bilateral administration of this dose of P in either VMH or vMES have a reliable effect. The results support the hypothesis that P action is required in both VMH and vMES to reliably stimulate receptivity in hamsters.

Animals↗
PubMed1991

Intracranial dialysis and microinfusion studies suggest that morphine may act in the ventromedial hypothalamus to inhibit female rat sexual behavior.

The present investigation examined the neural sites and mechanisms of opiate inhibition of female sexual behavior. Systemic administration of morphine (10 mg/kg) significantly reduced ovarian steroid-induced estrous behavior in female rats. This behavioral inhibition was prevented when the opiate receptor antagonist naloxone (5 mg/kg) was administered 30 min prior to morphine. Bilateral infusion of morphine directly into the ventromedial hypothalamus (VMH) also inhibited hormone-dependent estrous behavior for at least 2 hr. Furthermore, naloxone infusion into the VMH 20 min before behavior testing reduced the inhibitory effects of systemically administered morphine on lordosis. These results suggest that morphine may inhibit female sexual behavior by acting directly on the VMH, the primary site at which ovarian steroids facilitate this behavior. In a separate experiment we used in vivo brain microdialysis to test the hypothesis that morphine inhibits lordosis by interfering with norepinephrine (NE) neurotransmission in the VMH. In control rats, the onset of mating was associated with increased NE release in the VMH. Morphine-treated animals displayed neither behavioral estrus nor elevated NE release from the VMH when tested with stimulus males. These data are consistent with the hypothesis that morphine suppresses NE release in the VMH. Nevertheless, mechanisms other than or in addition to attenuation of hypothalamic NE release may contribute to the inhibitory effects of morphine on lordosis.

Animals↗