Induction Of Lordosis Research Articles

Estrous Cycle-Dependent Modulation of Sexual Receptivity in Female Mice by Estrogen Receptor Beta-Expressing Cells in the Dorsal Raphe Nucleus.

The sexual receptivity of female mice, shown as lordosis response, is mainly regulated by estradiol action on estrogen receptor alpha (ERα) and beta (ERβ), depending on the day of the estrous cycle. Previous studies revealed that ERα in the ventromedial nucleus of the hypothalamus (VMH) plays an essential role in the induction of lordosis on the day of estrus (Day 1). However, the mechanisms of the transition to nonreceptive states on the day after estrus (Day 2) are not completely understood. In the present study, we investigated the possible role of ERβ, which is highly expressed in the dorsal raphe nucleus (DRN), in lordosis expression. We found that ERβ-Cre female mice, which were ovariectomized and primed with estradiol and progesterone to mimic the estrous cycle, showed high levels of lordosis on Day 2 when ERβ-expressing DRN (DRN-ERβ+) neuronal activity was chemogenetically suppressed. This finding suggests that excitation of DRN-ERβ+ neurons is necessary for the decline of lordosis on Day 2. Fiber photometry recordings during female-male behavioral interactions revealed that DRN-ERβ+ neuronal activation in response to male intromission was significantly more prolonged on Day 2 compared with Day 1. Chemogenetic overstimulation of DRN-ERβ+ neurons induced c-Fos expression in brain areas known to be inhibitory for lordosis expression, even though they did not express anterogradely labeled fibers of DRN-ERβ+ cells. These findings collectively suggest that DRN-ERβ+ neuronal excitation serves as an inhibitory modulator and is responsible for the decline in receptivity during nonestrus phases.

Does transforaminal lumbar interbody fusion induce lordosis or kyphosis? Radiographic evaluation with a minimum 2-year follow-up.

Conflicting reports exist about whether transforaminal lumbar interbody fusion (TLIF) induces lordosis or kyphosis, ranging from decreasing lordosis by 3.71° to increasing it by 18.8°. In this study, the authors' aim was to identify factors that result in kyphosis or lordosis after TLIF. A single-center, retrospective study of open TLIF without osteotomy for spondylolisthesis with a minimum 2-year follow-up was undertaken. Preoperative and postoperative clinical and radiographic parameters and cage specifics were collected. TLIFs were considered to be "lordosing" if postoperative induction of lordosis was > 0° and "kyphosing" if postoperative induction of lordosis was ≤ 0°. A total of 137 patients with an average follow-up of 52.5 months (range 24-130 months) were included. The overall postoperative disc angle (DA) and segmental lordosis (SL) increased by 1.96° and 1.88° (p = 0.003 and p = 0.038), respectively, whereas overall lumbar lordosis remained unchanged (p = 0.133). Seventy-nine patients had lordosing TLIFs with a mean SL increase of 5.72° ± 3.97°, and 58 patients had kyphosing TLIFs with a mean decrease of 3.02° ± 2.98°. Multivariate analysis showed that a lower preoperative DA, lower preoperative SL, and anterior cage placement were correlated with the greatest increase in postoperative SL (p = 0.040, p < 0.001, and p = 0.035, respectively). There was no difference in demographics, cage type or height, or spinopelvic parameters between the groups (p > 0.05). Linear regression showed that the preoperative DA and SL correlated with SL after TLIF (R2 = 0.198, p < 0.001; and R2 = 0.2931, p < 0.001, respectively). Whether a TLIF induces kyphosis or lordosis depends on the preoperative DA, preoperative SL, and cage position. Less-lordotic segments became more lordotic postoperatively, and highly lordotic segments may lose lordosis after TLIF. Cages placed more anteriorly were associated with more lordosis.

The Effect of Anterior Cervical Discectomy and Fusion on Cervical Sagittal Vertical Axis and Lordosis with Minimum 2-Year Follow-Up

Anterior cervical discectomy and fusion (ACDF) can induce lordosis and improve cervical sagittal vertical axis (SVA), but multilevel ACDF may inadvertently increase cervical SVA because of insufficient lordosis induction. Patients who underwent 1-, 2-, or ≥3-level ACDF in the subaxial spine with minimum 2-year follow up were retrospectively studied. C2-C7 Cobb angle (lordosis), cervical SVA, and T1 slope were measured preoperatively, immediately postoperatively, and at last follow-up. Inclusion criteria were met by 127 patients. There were no differences in baseline demographics among 1-, 2-, and ≥3-level ACDF groups. Mean follow-up was 43.7 months (range, 24-142 months). Increase of cervical SVA immediately postoperatively was 1.94 mm,-1.44 mm, and 7.25 mm for 1-, 2-, and ≥3-level ACDF (P= 0.041) and at last follow-up was 2.97 mm, 0.70 mm, and 9.32 mm for 1-, 2-, and ≥3-level ACDF (P= 0.026). At last follow-up, 2-level ACDF patients had the greatest decrease in T1 slope (-0.43°) compared with increase of 2.71° for 1-level and 2.84° for ≥3-level patients (P= 0.028). In all 3 groups, segmental (ACDF levels) lordosis, cervical SVA, and T1 slope did not decrease from immediate postoperative to last follow-up. Only 2-level ACDF maintained C2-7 lordosis (2.16°) compared with loss of lordosis in 1-level (-0.84°) and ≥3-level (-2.00°) ACDF (P= 0.008) at last follow-up. Linear regression analysis showed that T1 slope had no relationship with correction of cervical SVA (P= 0.5310) but had a significant correlation with Cobb angle loss of C2-C7 lordosis (P= 0.0016). Compared with 1- and 2-level ACDF, ≥3-level ACDF resulted in significant increase of cervical SVA and loss of overall lordosis. Compared with 1- and ≥3-level ACDF, 2-level ACDF had the greatest ability to maintain lordosis. T1 slope had a significant correlation with loss of C2-C7 lordosis after ACDF.

Anterior Cervical Discectomy With Fusion and Plating for Correction of Degenerative Cervical Kyphosis: 2-Dimensional Operative Video.

This surgical video demonstrates the technique for correcting degenerative cervical kyphosis using an anterior cervical discectomy and fusion (ACDF). Degenerative cervical kyphosis can cause radiculopathy, myelopathy, and difficulty holding up one's head. The goal of surgical intervention is to alleviate pain, improve the ability for upright gaze, and decompress the spinal cord or nerve roots. Posterior-only approaches and anterior corpectomies are alternative treatments to address cervical kyphosis. However, an ACDF allows for sequential induction of lordosis via distraction over multiple segments and for further lordosis induction by sequential screw tightening, pulling the spine towards a lordotic cervical plate.1 This video shows 2 cases demonstrating a technique of correcting severe cervical degenerative kyphosis. The video illustrates our initial kyphotic Caspar pin placement coupled with sequential anterior distraction to correct kyphosis. The technique is most useful in patients who have good bone density, nonankylosed facets, and degenerative cervical kyphosis. We have received informed consent of this patient to submit this video.

Posterior Column Osteotomy of the Lumbar Spine: 2-Dimensional Operative Video.

The posterior column osteotomy (PCO) is a tool for correction in spinal deformity. It allows for the induction of lordosis and coronal plane correction. It can be performed at multiple levels to loosen and mobilize the spine. Although the PCO does not provide as much correction as a 3-column osteotomy, it can be done in less operative time and with less morbidity. Performing a PCO involves the resection of posterior bony elements, including entire facet complexes, the ligamentum flavum, and at least part of the lamina. The ligamentum flavum laterally is also resected, and the exiting nerve roots are skeletonized bilaterally. Compression of the osteotomy can cause foraminal stenosis, and it is important to ensure that the exiting nerve roots are adequately decompressed to avoid potential postoperative radiculopathy. The authors present an illustration of the technique with saw bones, a clinical case describing the use of PCOs, and an intraoperative video of a PCO performed at L5-S1. The patient consented to the surgical procedure and video/image recording for possible publication purposes prior to the operation being performed.

Anterior Column Realignment in Adult Spinal Deformity: A Case Report and Review of the Literature

Anterior column realignment (ACR) is a new emerging minimally invasive surgical technique for adult spinal deformity (ASD) that has the potential to provide similar corrective ability to traditional posterior approaches. This article reviews the current literature on the clinical efficacy and safety of ACR and illustrates an additional use of this technique in a case of sagittal imbalance after posterior spinal fusion with segmental instrumentation. We performed a literature search of all published ACR reports using PubMed, including only clinical studies describing the ACR technique and reporting radiographic and/or clinical outcomes. Thirteen studies were included. Improvement in lumbar lordosis after ACR ranged from 12.7° to 39°, and increases in focal segmental lordosis at each ACR level ranged from 1° to 34°. Good clinical and functional outcomes have consistently been reported after ACR. The complication rate has been comparable to or lower than traditional posterior-based techniques. We also illustrate the use of ACR in a patient with sagittal imbalance after a prior posterior instrumented spinal fusion. ACR in combination with a posterior osteotomy allowed for the induction of lordosis by cantilevering of rods and compression of pedicle screws. Radiographic and clinical outcomes after ACR have been promising so far. In addition to primary ASD surgery, ACR can also be effectively used in cases with prior posterior instrumented spinal fusion to correct sagittal imbalance.

Identification of neural cells activated by mating stimulus in the periaqueductal gray in female rats.

Induction of lordosis as typical female sexual behavior in rodents is dependent on a mount stimulus from males and blood levels of estrogen. Periaqueductal gray (PAG) efferent neurons have been suggested to be important for lordosis behavior; however, the neurochemical basis remains to be understood. In this study, we neuroanatomically examined (1) whether PAG neurons activated by mating stimulus project to the medullary reticular formation (MRF), which is also a required area for lordosis; and (2) whether these neurons are glutamatergic. Mating stimulus significantly increased the number of cFos-immunoreactive (ir) neurons in the PAG, particularly in its lateral region. Half of cFos-ir neurons in the lateral PAG were positive for a retrograde tracer (FluoroGold; FG) injected into the MRF. cFos-ir neurons also colocalized with mRNA of vesicular glutamate transporter 2 (vGLUT2), a molecular marker for glutamatergic neurons. Using retrograde tracing and in situ hybridization in conjunction with fluorescent microscopy, we also found FG and vGLUT2 mRNA double-positive neurons in the lateral PAG. These results suggest that glutamatergic neurons in the lateral PAG project to the MRF and are involved in lordosis behavior in female rats.

Membrane-Initiated Estrogen Actions on Ion Channels and the Induction of Lordosis, the Rodent Female Sexual Behavior

The explosive increase of research in ”membrane-initiated” (also called ”non-genomic” or ”rapid” or ”acute”) estrogen actions in the past ten years not only established them as legitimate but also showed that they can activate many signaling pathways that can lead indirectly or even directly to the modulation of genomic functions. The latter raised the possibility that estrogens' membrane-initiated actions can synergize with their genomic actions. We have turned this possibility into a reality by first using cultured cells and then whole animals. With cultured neuroblastoma and MCF-7 breast cancer cells, we demonstrated that membrane-initiated estrogen actions could facilitate subthreshold doses of estradiol to accomplish a transcriptional facilitation, and found that the facilitation was mediated, at least in part, by pathways involving PKA and PKC. Using the estrogen-dependent rodent female sexual behavior, lordosis, as a study model, we found that implantation of a membrane-impermeable estrogen, which by itself could not induce the behavior, in the hypothalamic ventromedial nucleus (VMN) of female rats facilitated subthreshold estradiol similarly implanted later to induce lordosis. These findings, to our knowledge, comprise the first demonstration of the synergism between estrogen's membraneinitiated and genomic actions. Consistent with our cell culture studies, the facilitation of lordosis induction also required functioning PKA and PKC. Several lines of evidence indicated that an increase in neuronal activity during the initial stage of estrogen administration is required for the induction of lordosis. Therefore, whether the activity of VMN neurons is modulated by the membrane-initiated actions of the estrogen applied to the hypothalamus was investigated. With extracellular single-neuron recording of VMN cells in hypothalamic slices of female rats, it was found that acutely applied estradiol (acute E2) could i) potentiate the excitation mediated by two distinct types of receptors, G protein-coupled excitatory histamine (HA) receptors and NMDA ion channel/receptors, and ii) attenuate inhibition caused by G protein-coupled inhibitory HA receptors. These findings raised the possibility that acute E2 can potentially working through three independent mechanisms to modulate these responses. This possibility was evaluated using whole cell patch clamp studies. Corresponding to extracellular recording findings, HA could evoke de- and/or hyper-polarization, and NMDA could evoke only depolarization. Acute application of E2 could, again, potentiate HA and NMDA depolarization and attenuate HA hyperpolarization. To search for mechanisms, pharmacological analyses of HA responses were performed to define receptors responsible for excitation and inhibition, and effects of acute E2 on individual types of HA receptors were studied. Results from these studies, together with current knowledge about HA receptors, point to a likely mechanism underlying non-genomic estrogen modulations of HA responses: acute E2 inhibits K(superscript +) channels through the facilitation of G(subscript q/11) coupled to histaminergic H1 receptors, to potentiate HA depolarization/ excitation as well as to attenuate hyperpolarization/inhibition. We also searched for mechanism(s) underlying acute E2 potentiation of NMDA depolarization/excitation by characterizing NMDA actions. We found that both NMDA and acute E2 could reduce afterhyperpolarizations, which are mediated by Ca(superscript ++)-activated K(superscript +) channels. Therefore, attenuation of these channels appears to be one way acute E2 can potentiate NMDA depolarization/excitation. Thus, in the induction of lordosis at least, membraneinitiated non-genomic estrogen actions appear to facilitate genomic actions by both activating signaling pathways involving PKA and PKC and by inhibiting certain K(superscript +) channels.

Hormonal induction of lordosis and ear wiggling in rat pups: gender and age differences

To assess how early can estrogens induce female mating behaviors, rat pups 8-29 days old (D8-D29, respectively) were injected twice daily with estradiol benzoate (E) or oil (O) followed by progesterone (P) or oil, and then observed for the estrogen-dependent ear wiggling (EW) and lordosis in response to natural stimulation from male rats. In female pups treated with E + E + P, the incidence of EW appeared as early as D13 and increased gradually to reach maximum at D18, when all pups tested showed EW. EW also occurred in E + E + O females, but never in O + O + P females or in any E + E + P male. Lordosis in E + E + P, as well as E + E + O, female pups occurred later, starting at D15. O + O + P females or E + E + P males never display lordosis. To explore the possibilities that the age and gender differences are due to distribution and/or function of estrogen receptor-alpha (ERalpha) or progesterone receptor (PR), separate pups were used for immunocytochemical (ICC) staining of these receptors in the hypothalamic ventromedial nucleus (VMN). There was no age difference in female pups in the density of ERalpha or the induction of PR between D11/D12, when no sexual behavior was observed, and D19/D20, when almost all pups tested performed the behaviors. There were gender differences: male pups had less ERalpha than females at D19/D20, though not at D11/D12, and did not respond to E in the induction of PR in the VMN. These results show that ERs and their signaling systems in the VMN of rat pups are functional at least after D11 but only in females, and that the gender differences appeared to be due to differences in the molecular biology of ERalpha.

Acute estrogen potentiates excitatory responses of neurons in rat hypothalamic ventromedial nucleus

In a previous behavioral study, brief application of a membrane-limited estrogen to neurons in rat hypothalamic ventromedial nucleus (VMN) facilitated lordosis behavior-inducing genomic actions of estrogen. Here, electrophysiological recordings from single neurons were employed to characterize these membrane-initiated actions. From rat hypothalamic slices, electrical activity was recorded from neurons in the ventrolateral VMN, the cell group crucial for estrogen induction of lordosis. In addition to the resting activity, neuronal responses to histamine (HA) and N-methyl- d-aspartate (NMDA) were also recorded before, during, and after a brief (10–15 min) application of estradiol (E, 10 nM). These two transmitters were chosen because their actions are mediated by different mechanisms: HA through G protein-coupled receptors and NMDA by ligand-activated ion channels. Vehicle applications did not affect either resting activity or neuronal responses. In contrast, acute E exposure modulated neuronal responses to transmitters, with no significant effect on the resting activity. It potentiated excitatory responses to HAs (20 out of 48 cells tested) and to NMDA (10 out of 19 cells), but attenuated inhibitory responses to HA (3 out of 6 units). Both of these hormonal actions would increase VMN neuronal excitation. In separate experiments, neuronal excitation was found to be suppressed by anesthetics, which would block E's induction of lordosis when administered at the time of estrogen application. These data are consistent with the notion that increasing electrical excitation of VMN neurons can be a mechanism by which acute E exposure facilitates the lordosis-inducing genomic actions of estrogens.

Suppressive effect of neonatal treatment with a phytoestrogen, coumestrol, on lordosis and estrous cycle in female rats

The neural control systems for the ovulatory cycle and lordosis behavior are sexually differentiated by estrogen during the perinatal period in rats. In the present study, the effects of a single neonatal injection with the phytoestrogen, coumestrol, on female reproductive functions were investigated. Female rats were injected subcutaneously with 1 or 3 mg coumestrol (CM1, CM3), 1 mg genistein (GS1), 1 mg estradiol (E 2), or oil at day 5 after birth (birth day = day 1) and an estrous cycle check and lordosis behavior test were performed. As a result, vaginal opening was advanced in CM1-, CM3- or E 2-treated females. A vaginal smear check indicated that oil- or GS1-treated females showed a constant 4- or 5-day estrous cycle, whereas CM1-, CM3- or E 2-treated rats showed a persistent or prolonged estrus. Ovariectomy was performed in all females at 60 days of age. The ovary weights in the CM1-, CM3- or E 2-treated groups were lower than those in the oil- and GS1-treated groups and no corpora lutea were found in any rats of these three groups, except for two E 2-treated rats. Behavioral tests were carried out after implantation of E 2-tubes. All rats in the CM1-, GS1-treated groups showed a high lordosis quotient (LQ), being comparable to that in the oil-treated females. On the other hand, LQs in the CM3, E 2 or male groups were lower than that in the control female group. These results suggest that a single neonatal injection of 3 mg coumestrol was effective in suppressing the functions of ovulation-inducing mechanisms and the induction of lordosis, but 1 mg coumestrol was effective in only the estrous cycle of female rats.

Lordosis induction in juvenile red sea bream, Pagrus major, by high swimming activity

Lordosis is correlated with absence or malfunction of the swimbladder. However, swimbladder abnormalities do not completely explain the occurrence of lordosis. We examined whether muscle activities from vigorous tail beat induced by removal of the caudal fin could induce lordotic malformation in juvenile red sea bream. We also attempted to determine the minimal current velocity for inducing lordosis in relation to total length (TL). For this purpose, we employed relative current velocity in terms of “move of water in times of total body length per second (TL s −1)”. We compared effects of different water current (2 vs. 4 TL s −1) for 10 days on bone malformation using juvenile of 25-mm TL. Exposure to 4 TL s −1 current velocity, but not 2 TL s −1, induced lordosis. Lordotic juvenile red sea bream had a cuneiform centrum mainly at the 15th vertebra. Lordosis was observed in fish with normal swimbladders as well. Thus, swimbladder abnormalities alone cannot completely explain the occurrence of lordosis. We removed part or all of the caudal fins of fish of 40-mm TL and exposed these fish to 2 TL s −1 current for 10 days. Control fish did not show deformations in the vertebrae. Fish with complete removal of the caudal fin swam with vigorous tail beats. However, fish with complete, upper or lower caudal fin removal (36%, 29% or 7%, respectively) displayed lordosis even at the current velocity of 2 TL s −1. These findings suggested that the muscle activities from excess beat of the tail against excessive current, but not the mechanical action of the caudal fin, induced lordosis.

Intravenous progesterone elicits a more rapid induction of lordosis in rats than does SKF38393

In ovariectomized (ovx), estradiol (E)-primed rats, progesterone (P) facilitates sexual receptivity within 2–30 min following intravenous (i.v.) administration. Intracerebroventricular infusion of P or the dopamine receptor type 1-like (D1) agonist, SKF38393, increases lordosis in ovx, E-primed rats, and intracellular progestin receptor (PR) blockers attenuate P and SKF38393’s facilitation of lordosis. The present experiments examined whether P can have effects via Dl receptors and compared the onset of P’s and SKF38393’s induction of lordosis following i.v. administration. Ovx rats (N = 20) with i.v. jugular catheters were primed daily with 2 µg E subcutaneously and were pretested for sexual receptivity. In Experiment 1, rats (n = 10) were repeatedly tested for receptivity 3–7, 15, 30, 60, and 120 min following i.v. infusion of P (2 µg), SKF38393 (100 ng), and propylene glycol vehicle (0.2 cc). Progesterone increased postinfusion lordosis at all test times, whereas SKF38393’s increases in lordosis were not statistically significant until 15 min following i.v. infusion, relative to lordosis following vehicle or pretest conditions in Experiment 1. In Experiment 2, rats (n = 15; 5 from Experiment 1, and 10 new subjects) received infusions of the antiprogestin, RU38486, the D1 antagonist, SCH23390, or vehicle followed by a second P or vehicle infusion. Although both RU38486 and SCH23390 blocked the facilitatory effects of P on lordosis, their effects varied. RU38486 completely blocked P’s effects, whereas SCH23390 did not. In Experiment 3, rats (n = 15, from Experiment 2) received infusions of RU38486, SCH23390, or vehicle followed by a second SKF38393 or vehicle infusion. RU38486 and SCH23390 both effectively blocked the facilitatory effects of SKF38393 on lordosis. In Experiment 4, rats (n = 15, from Experiment 3) received i.v. infusions of P, which rapidly and significantly increased the number of super-threshold spikes in the ventral tegmental area, but not in the ventral medial hypothalamus or in the parietal cortex. These data suggest that actions at intracellular progestin receptors do not account for all of P’s effects to facilitate receptivity. Interestingly, although PRs may be involved in P and D1 ligand’s activation of female sexual behavior, D1 receptors are not required for P’s effects. However, i.v. P rapidly and significantly alters neuronal activity in sites with the greatest concentration of dopamine neurons (ventral tegmental area > ventral medial hypothalamus > cortex).

Dopaminergic Regulation of Progesterone Receptors: Brain D5 Dopamine Receptors Mediate Induction of Lordosis by D1-Like Agonists in Rats

To characterize the signaling pathway by which the neurotransmitter dopamine modulates progesterone receptor (PR) activation, the steroid-dependent behavior lordosis was used in estrogen-primed ovariectomized Sprague-Dawley rats with stereotaxic implanted third ventricle cannulas. Lordosis was observed in response to solicitous males in females after central administration of the D1-like agonist SKF38393 and three of its analogs (SKF77434, SKF75640, and SKF85174). In contrast, D1-like antagonist SCH23390 and D1-like/D2 repopulation inhibitor EEDQ blocked behavior inducible by the D1-like agonists. Further, antisense oligonucleotides to D5, but not D1, dopamine receptor mRNA suppressed reproductive behavior associated with D1-like stimulation. This finding provides strong evidence that dopaminergic modulation of lordosis is mediated by the novel D5 dopamine receptor. Although D1, but not D5, dopamine receptor mRNAs were detected in the ventromedial nucleus (VMN) by in situ hybridization, agonists microinjected into the VMN, but not into the arcuate nucleus or preoptic area, induced lordosis, suggesting the functional presence of D5 dopamine receptors in the VMN. Also in support, D5 receptor mRNA antisense microinjected into the VMN blocked the subsequent induction of lordosis by D1-like agonists. Finally, facilitation of sex behavior by D1-like agonists was blocked by the antiprogestin RU38486 and PR antisense oligonucleotide. Collectively, the data provide strong evidence for dopaminergic modulation of reproductive behavior through D5 dopamine receptor-mediated modulation of PR-dependent behavior in rat CNS.

In vivo evidence for progesterone dependent decreases in serotonin release in the hypothalamus and midbrain central grey: relation to the induction of lordosis

The effects of progesterone (P) on serotonin (5HT) overflow in the ventromedial hypothalamus (VMH), preoptic area (POA) and midbrain central grey (MCG) were studied using in vivo microdialysis. Ovariectomized rats, pretreated with 5 μg estradiol, were anesthetized with chloral hydrate and stereotaxically implanted with dialysis probes directed towards one of the respective brain sites. Extracellular 5HT levels stabilized 3 to 5 h following probe implantation. Under stable baseline conditions, perfusion of 1 μM tetrodotoxin through the dialysis probe resulted in a 60–65% reduction in 5HT overflow in the brain areas studied. In experiments testing the effect of P on 5HT overflow, rats were subcutaneously injected with 0.5 mg P or propylene glycol vehicle. Samples were analyzed for 5HT at 20 min intervals for 4 h after treatment. Perfusate levels of 5HT were not significantly changed in the VMH, POA or MCG in vehicle-treated rats. Similarly, P treatment failed to significantly alter 5HT overflow in the POA. In the VMH, perfusate levels of 5HT were significantly reduced 60 min after P treatment. Decreases in perfusate 5HT levels were detected 20 min after P in the MCG. The decreases in 5HT overflow measured in the VMH and MCG following P treatment persisted for the remainder of the sampling period with the exception of 1 time point in the VMH. The results provide in vivo evidence for P-influenced decreases in 5HT release in the VMH and MCG. The rapid decrease in extracellular 5HT in the MCG suggests that this effect may represent a non-genomic action of P. These results are discussed in relation to the role of 5HT in the regulation of lordosis behavior.

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.

Progesterone facilitates lordosis, but not LH release, in estradiol pulse-primed male rats

Gonadectomized (GDX) male and female rats received repeated cycles of estradiol pulses, which prime animals of both sexes to display progesterone-facilitated lordosis. One, three and six treatment cycles of estradiol pulses followed by progesterone induced progressively higher luteinizing hormone (LH) surges in GDX females. Six treatment cycles of estradiol pulses alone (i.e., without subsequent progesterone treatment) induced a small but significant (∼4 ng/ml) increase in LH levels in GDX females. In contrast, GDX males never produced LH surges in response to estradiol pulses alone or estradiol pulses followed by progesterone, regardless of the number of hormone treatment cycles. Thus, female patterns of steroid-induced sexual receptivity and LH release are not inextricably linked, as steroid treatments sufficient for induction of lordosis do not stimulate LH secretion in adult male rats. These data also suggest that the neural system governing the LH surge might be more firmly sexually differentiated than that responsible for sexual receptivity in rats.

Chemical structure of corticosteroids and its relationship with their acute induction of lordosis in the female rat

The intravenous injection of several corticosteroids in the spayed estrogenprimed rat resulted, 5 min later, in a remarkable induction of lordosis response for deoxycorticosterone and 11-deoxycortisol. A lower but important effect was induced with corticosterone and 17α-hydroxyprogesterone. A chemical structure-biological effect analysis showed that C-21 hydroxylation (e.g., deoxycorticosterone, 11-deoxycortisol, and corticosterone) induces the behavioral effect. However, C-11 or C-17 hydroxylation alone promotes the lordosis response to a lesser degree (corticosterone and 17α-hydroxyprogesterone, respectively). However, the effect of these latter compounds is significant. From the results, it is concluded that deoxycorticosterone and 11-deoxycortisol along with other steroids such as 20α-hydroxyprogesterone are suitable candidates for synergizing the well-known estrogen-progesterone induction of lordotic behavior.

Changes in hypothalamic neuronal function related to hormonal induction of lordosis in behaving hamsters

The hypothalamus is known to be critical for the neuroendocrine control of sexual behavior, but the neural effects of gonadal hormones on behavior-related activity of hypothalamic neurons has received little investigation. The present study examined the effects on single hypothalamic neurons of lordosis-inducing estrogen and progesterone administration to behaving golden hamsters. The lordosis-inducing action of the hormones was associated with rapidly emerging, cumulative changes in the activity level and somatosensory responsiveness of neurons throughout the hypothalamus, as well as the appearance in most neurons of lordosis-correlated firing. This functional reconfiguration of hypothalamic neuronal properties resembled, in time course and other aspects, effects of estrogen and progesterone previously observed in hamster midbrain neurons. Although the firing rates of the hypothalamic neurons were typically low, the lordosis-related activity of these neurons was compatible with a role in the control of individual episodes of lordosis as well as a state-related tendency to exhibit the lordosis response.

Nerve growth factor-mediated sexual differentiation of the rat hypothalamus

Injection of antibody to nerve growth factor into the cerebral lateral ventricle blocked testosterone-induced behavioral defeminization of neonatal female rats. When tested as adults following ovariectomy and combined estrogen-progesterone treatment, the injected animals showed a significantly higher lordosis quotient than the testosterone-treated, normal rabbit serum-infused controls. Failure of vaginal opening and clitoral enlargement manifested the well-documented masculinizing effect of testosterone on the genitalia in the experimental as well as the control animals. Estrogen sensitivity of hypothalamic neurons which are responsible for the induction of lordosis was retained in the experimental animals. Recordings of the antidromic action potentials from neurons in the ventromedial nucleus of the hypothalamus following stimulation of the midbrain central gray revealed that estrogen decreased the antidromic activation threshold and shortened the absolute refractory period of the hypothalamic efferents along with the estrogen-induced behavioral activation in the experimental animals. In the control group, the estrogen-induced neuronal activation was lost altogether with the behavioral activation.