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Effect of 5 alpha-dihydrotestosterone and flutamide on the facilitation of lordosis by LHRH and naloxone in estrogen-primed female rats.

Although 5 alpha-dihydrotestosterone (DHT) is a potent inhibitor of lordosis behavior in ovariectomized estrogen-primed female rats, the mechanism(s) by which this steroid has this action is unknown. The present experiments sought to determine whether DHT inhibits lordosis by preventing the known facilitatory actions of luteinizing hormone-releasing hormone (LHRH), naloxone, and Substance P on lordosis. Lordosis behavior was examined in ovariectomized, estrogen-primed rats prior to or 30, 60, 90, and 180 min following intracerebroventricular (ICV) infusion of LHRH (500 ng), naloxone (1 microgram). Substance P (1 microgram), or saline and 0.01 N acetic saline vehicles, and the effects of DHT (2.5 mg/rat) following similar treatment were examined. In Experiment 1, LHRH and naloxone increased lordosis within 30 min after infusion, while Substance P and the saline or acetic saline vehicles had no effect. Treatment with DHT in combination with estrogen prevented the facilitation of lordosis by LHRH and naloxone. In Experiment 2, ovariectomized, estrogen-primed females shown to be responsive to LHRH during a first screening test were tested for lordosis after receiving either DHT or DHT in combination with the androgen receptor antagonist, Flutamide (7.5 mg/injection x 3). Again, DHT prevented the facilitatory action of LHRH; however, Flutamide did not counteract that effect. In Experiment 3, Flutamide did not counteract the inhibitory effect of DHT on estrogen and progesterone-induced lordosis. These results demonstrate that the inhibitory effect of DHT cannot be overridden by neuroactive peptides which themselves stimulate receptivity. It seems unlikely that DHT inhibits lordosis either by interfering with the behavioral action of these peptides or by activation of the androgen receptor.

Anilides↗

Dual effect of morphiceptin on lordosis behavior: possible mediation by different opioid receptor subtypes.

Intracerebroventricular (ICV) infusions of the selective mu receptor agonist morphiceptin produce a dual effect on lordosis behavior in ovariectomized, steroid-primed rats. Low doses of morphiceptin (20 ng) inhibit lordosis whereas higher doses (2000 ng) facilitate this behavior. The present experiment tested whether naloxone, an antagonist of both high- and low-affinity mu receptors, or the long-acting high-affinity mu receptor antagonist naloxazone could block the dual effect of morphiceptin on lordosis. Ovariectomized rats primed with estrogen and progesterone received naloxone, naloxazone, or a control solution prior to ICV infusions of either 0, 20, or 2000 ng of morphiceptin. Naloxone reversed both the inhibition and facilitation of lordosis produced by morphiceptin, but had no effect on lordosis when administered before control infusions. In contrast, naloxazone reversed the inhibition but not the facilitation of lordosis. These results indicate that the inhibitory effect of morphiceptin on lordosis reflects the activation of high-affinity mu receptors whereas the facilitatory effect reflects either the activation of low-affinity mu receptors or other opioid receptor subtypes. The failure of naloxone or naloxazone to affect lordosis in rats receiving control infusions of saline further suggests that endogenous opioid systems do not exert a tonic inhibitory or facilitatory action on lordosis behavior.

Analgesics↗

Effects of tegmental lesions on lordosis and body weight in female hamsters.

Lordosis responses in naturally-estrous hamsters were elicited by unilateral manual stimulation. Response latencies were compared before and after unilateral lesions of medial and lateral tegmental areas located ventral and ventrolateral, respectively, to the midbrain central gray. The only significant effects were produced by the more lateral lesions. These caused slightly delayed lordosis responses to stimulation of the ipsilateral flank, but had much more pronounced effects on responsiveness to contralateral stimuli, which often entirely failed to elicit lordosis postlesion. This difference in the effectiveness of ipsi- and contralateral stimuli suggests a selective disruption of neural mechanisms involved in the somatosensory control of lordosis initiation. Its locus suggests that a similar mechanism previously identified in the hamster tectum extends ventrally into the dorsal tegmentum, where it overlaps areas implicated in the sensory control of lordosis in other rodents. Since unilateral lesions of the dorsomedial tegmentum failed to affect behavior, a second experiment tested the effects of bilateral medial lesions on male-stimulated lordosis responses in ovariectomized, hormone-primed hamsters. These lesions caused significant increases in body weight, but again failed to show direct effects on lordosis. This result helps to delimit a ventral tegmental system previously implicated in the control of lordosis maintenance in hamsters. In addition, it suggests species differences in the brain circuits involved in the motor control of lordosis.

Analysis of Variance↗

Facilitation of female rat lordosis behavior by hypothalamic infusion of 5-HT(2A/2C) receptor agonists.

Ovariectomized rats were hormonally primed with 0.5 microg estradiol benzoate and 500 microg progesterone to produce two groups of rats differing in their lordosis behavior. Females with a lordosis to mount (L/M) ratio < 0.5 were used to test the hypothesis that 5-HT(2A/2C) receptor agonists could facilitate lordosis behavior. Females with L/M ratios > or = 0.5 were used to evaluate the potential suppressive effect of 5-HT(2A/2C) receptor compounds. Lordosis behavior was examined following bilateral infusion of drugs into the ventromedial nucleus of the hypothalamus (VMN). Drugs examined were the 5-HT(2A/2C) receptor agonist, (+/-)-1-(2,5-dimethoxy-4-iodophenyl)-2-aminopropane HCl (DOI), the 5-HT(2A/2C) receptor antagonist, 3-[2-[4-(4-fluorobenzoyl)-1-piperdinyl]ethyl]-2,4(1H,3H)-quinazoli nedione tartrate (ketanserin tartrate), and the non-selective 5-HT receptor agents, 2-(1-piperazinyl)quinoline dimaleate (quipazine) and N-(3-trifluoromethylphenyl)piperazine HCl (TFMPP). Drugs with agonist action at 5-HT(2A/2C) receptors increased lordosis behavior in rats with low sexual receptivity. The 5-HT(2A/2C) receptor antagonist, ketanserin, inhibited lordosis behavior in sexually receptive rats. DOI attenuated the lordosis-inhibiting effect of ketanserin, but ketanserin was less effective in preventing DOI from increasing lordosis behavior. These results strengthen prior inferences that activation of 5-HT(2A/2C) receptors can facilitate lordosis behavior and that the VMN is one site at which such facilitation can occur.

Amphetamines↗

Differential effects of beta-endorphin and Met- and Leu-enkephalin on steroid hormone-induced lordosis in ovariectomized female rats.

The effect of intrathirdventricular (I.T.V.) injections of beta-endorphin, anti-beta-endorphin antiserum, Met-enkephalin, Leu-enkephalin, and naloxone on the initial activation and final development of steroid hormone-mediated induction of female sexual receptivity was studied in ovariectomized female rats. The lordosis response to male mounts in ovariectomized rats after subcutaneous (S.C.) estradiol benzoate (EB) and progesterone (Prog) priming was facilitated by beta-endorphin, and Met-enkephalin (10 microg x 5 microl(-1)), but inhibited by Leu-enkephalin, when the peptides were injected into the third ventricle at the time of S.C. EB priming. A lower dose Met-enkephalin had no effects. Lordosis behavior in steroid hormone-primed rats was significantly facilitated when I.T.V. injections of Met-enkephalin were given 1 h prior to behavioral testing (47 h after EB priming). At 1 h prior to behavioral testing (47 h after EB priming), I.T.V. injection of beta-endorphin significantly inhibited lordosis behavior, especially at the higher dose of beta-endorphin (10 microg x 5 microl(-1)). Under those conditions, Leu-enkephalin had no effect. Lordosis behavior of ovariectomized female rats receiving S.C. steroid hormones and I.T.V. injection of anti-beta-endorphin antiserum was significantly inhibited when anti-beta-endorphin antiserum was injected at the time of EB priming. However, lordosis was significantly facilitated when anti-beta-endorphin antiserum was injected 1 h prior to the behavior testing (47 h after EB priming). In contrast, I.T.V. injection of the opioid antagonist naloxone given either at the time of EB priming or 1 h prior to behavioral testing (47 h after EB priming) decreased lordosis behavior. The present results suggest that 1) beta-endorphin, Met-enkephalin, and Leu-enkephalin have differential effects in the control of lordosis behavior; 2) the opioidergic systems may modulate initial-stage and final-stage estrogen-induced lordosis behavior; and 3) the opioidergic systems could be divided into the endorphinergic modulation-type and enkephalinergic modulation-type, based on their effects on lordosis behavior.

Animals↗

Coordination between the lumbar spine lordosis and trunk angle during weight lifting.

OBJECTIVE: To analyze the coordination of the lumbo-sacral angle (lumbar spine lordosis) and the trunk inclination during lifting of different loads. STUDY DESIGN: Kinematic data of spine motion were analyzed. The parameters characterizing the relationships between the lordosis and the trunk inclination angle were estimated. BACKGROUND: The shape of the spine has been analyzed mostly for static or quasi-static conditions. The parameters relating the lumbar spine lordosis and trunk inclination in dynamics have not been analyzed. METHODS: Healthy subjects performed unconstrained weight lifts from ground to mid-thigh level. Kinematic data were derived from the tracking of markers (light-emitted diodes) placed over the spine and pelvis using an OPTPTRAK system. The relationship between lordosis and trunk inclination was analyzed. RESULTS: The relationship between lumbar spine curvature (lumbo-sacral angle or lordosis) and trunk inclination during weight lifting was described by an exponential function with three parameters. These were the lordosis extremes associated with the horizontal and vertical positions of the trunk and the trunk inclination when lordosis equals zero. The absolute value of the lordosis angle decreases at the onset of the extension phase of lifting when the load increases, implying active reaction of musculosceletal system to increasing load. CONCLUSIONS: The changes in the lordosis and trunk inclination are strictly correlated implying that the nervous system actively coordinates the degrees of freedom of the spine, providing an inter-joint synergy.

Journal Article↗

Lordosis of rats is modified by neurosteroidogenic effects of membrane benzodiazepine receptors in the ventral tegmental area.

Progestins modulate lordosis through actions in the ventral tegmental area (VTA). Whether neurosteroidogenesis of 5alpha-pregnan-3alpha-ol-20-one (3alpha,5alpha-THP), involving mitochondrial benzodiazepine receptors (MBR), is important for lordosis was investigated. Ovariectomized (Ovx), hormone-primed rats (experiments 1, 3, 5, 6) and rats in behavioral estrus (experiments 2 and 4) were unilaterally infused via chronic guide cannula to the VTA with a MBR agonist, N,N-dihexyl-2-(4-fluorophenyl) indole-30-acetamide (FGIN 1-27) or antagonist 1-(2-chlorophenyl)-N-methyl-N-(1-methylpropyl)-3-isoquinolinecarboximide (PK-11195). Experiment 1: Estradiol benzoate (EB)-primed (25 microg) rats administered 0 or 25 microg progesterone (P4) SC showed increased lordosis when infused with 5.0 microg FGIN 1-27 to the VTA; those administered 100 or 200 microg P4 SC exhibited greater lordosis when infused with 2.5 or 5.0 microg FGIN, relative to saline-infused rats. Experiment 2: Rats, near the termination of behavioral estrus, infused with 2.5 or 5.0 microg of FGIN 1-27 to the VTA, showed increased lordosis compared to that seen following vehicle administration. Experiment 3: EB-primed rats administered 200 or 500 microg P4 SC showed decreased lordosis when infused with 100, 200, or 400 ng PK-11195, relative to saline-infused rats. Experiment 4: Rats infused at the peak of behavioral estrus with 100, 200, or 400 ng PK-11195 to the VTA exhibited reduced lordosis compared to that seen following vehicle administration. Experiment 5: 3alpha,5alpha-THP (100 ng) infusions to the VTA reinstated lordosis of hormone-primed rats infused with PK-11195 (100 ng) to the VTA. Experiment 6: FGIN 1-27 (5.0 microg) and PK-11195 (100 ng) infusions aimed at the VTA respectively increased and decreased midbrain levels of 3alpha,5alpha-THP compared to vehicle. Notably, the specific effects observed with infusions to the VTA were not seen with infusions to the control site, the substantia nigra. These data suggest that neurosteroidogenesis involving MBRs in the VTA mediates lordosis of hormone-primed or behavioral estrous rats.

5-alpha-Dihydroprogesterone↗

In the ventral tegmental area, G-proteins and cAMP mediate the neurosteroid 3alpha,5alpha-THP's actions at dopamine type 1 receptors for lordosis of rats.

Progestins have multiple mechanisms of action in the central nervous system that are important for modulating lordosis of female rats. In the ventral tegmental area (VTA), progestins, such as the progesterone metabolite and neurosteroid 5alpha-pregnan-3alpha-ol-20-one (3alpha,5alpha-THP), regulate lordosis via actions independent of intracellular progestin receptors. We hypothesized that if, in the VTA, dopamine type 1 receptors (D1), G-proteins, and adenosine 3',5'-monophosphate (cAMP) are downstream effectors of 3alpha,5alpha-THP's actions for lordosis, then pharmacological manipulations of these signaling molecules will produce changes in 3alpha,5alpha-THP-facilitated lordosis of estradiol (E2)-primed rats. VTA infusions of 3alpha,5alpha-THP (50 ng) or 3alpha,5alpha-THP and the D1 agonist SKF38393 (100 ng) increased lordosis of ovariectomized, E2 (10 microg)-primed rats, compared to vehicle. Both 3alpha,5alpha-THP- and 3alpha,5alpha-THP plus SKF38393-facilitated lordosis was reduced by VTA infusions of the G-protein inhibitor guanosine 5'-O-(2-thiodiphosphate) (GDP-beta-S; 50 microM), but not vehicle. Also, in the VTA, blocking D1 with SCH23390 (100 ng) decreased, or increasing cAMP with 8-bromo-cAMP (200 ng) enhanced, 3alpha,5alpha-THP-facilitated lordosis of E2-primed rats. Notably, SCH23390's inhibitory effects on 3alpha,5alpha-THP-facilitated lordosis were reversed by 8-bromo-cAMP. Thus, in the VTA, 3alpha,5alpha-THP's actions for lordosis may involve activation of D1 and initiation of the G-protein-mediated second messenger cAMP.

2,3,4,5-Tetrahydro-7,8-dihydroxy-1-phenyl-1H-3-ben↗

Regulation of lordosis by cyclic 3',5'-guanosine monophosphate, progesterone, and its 5alpha-reduced metabolites involves mitogen-activated protein kinase.

Progesterone (P) and its ring A-reduced metabolites regulate sexual behavior in ovariectomized, estrogen-primed female rats when they are administered intracerebrally and systemically. The present study tested the hypothesis that the MAPK pathway participates in P facilitation and sequential inhibition of sexual behavior. The role of MAPK in lordosis facilitation by two ring A-reduced metabolites of P, 5alpha-dihydroprogesterone (5alpha-DHP) and 5alpha,3alpha-pregnanolone (5alpha,3alpha-Pgl), was also assessed. In Experiment 1, the MAPK inhibitor PD98059 was infused intracerebroventricularly before progestin administration. Lordosis behavior induced by P, 5alpha-DHP, and 5alpha,3alpha-Pgl was abolished 2 h after progestin administration by PD98059. P and 5alpha,3alpha-Pgl facilitation of proceptive behaviors was also decreased by the MAPK inhibitor. Experiment 2 examined the effects of MAPK inhibition on P sequential inhibition. Estrogen-primed females received intracerebroventricular infusions of PD98059 or vehicle 30 min before systemic administration of P and were tested for lordosis 4 h later. Animals received a second injection of P 24 h later and were retested for lordosis. The MAPK inhibitor blocked both lordosis facilitation and sequential inhibition produced by systemic administration of P. Because cGMP can also facilitate lordosis behavior, and cGMP-dependent protein kinase can activate MAPK, experiment 3 determined whether interference with MAPK would affect cGMP enhancement of lordosis. The icv infusion of PD98059 significantly inhibited lordosis behavior induced by 8-bromo-cGMP, a cell-permeable cGMP analog, at both 2 and 4 h. These data support the hypothesis that the MAPK pathway is involved in lordosis regulation by P and some of its ring A-reduced metabolites as well as by the second messenger, cGMP.

5-alpha-Dihydroprogesterone↗

[A study of urinary immunoglobulins and electrolyte excretion after lordosis].

We described a transient low or non-selective proteinuria after forced lordosis as a characteristic of orthostatic proteinuria and the heteroporous theory and sieving function theory which might explain the mechanism of orthostatic proteinuria. The angiogenic action of the renin-angiotensin system played an important part in these theories. Angiotensin II was recognized as the key regulator of renal sodium excretion, because it reduced the urinary Na/K ratio. Since the purpose of this study is to investigate the influence of the renin-angiotensin system on the mechanism of orthostatic proteinuria, proteins and electrolytes in the urine were examined before and after lordosis in 9 healthy children (Group A) and in 6 children with orthostatic proteinuria (Group B). The urinary ratio of protein/creatinine (P/cre) in Group B was already significantly higher than that in Group A before lordosis and significantly increased after lordosis, while P/cre in group A did not increase after lordosis. The urinary Na/K ratio (Na/K) in Group B was already significantly lower than that in Group A before lordosis, and after forced lordosis, Na/K in Group A decrease with no difference between both groups observed. It is suggested that a significant increase on P/cre after lordosis was obtained only in Group A, whereas in both groups the renal vein may be compressed by forced lordosis and as a result angiotensin II may be stimulated. There might be a difference of the responsibility to angiotensin II in glomerular mesangium contraction between both groups.

Adolescent↗

In the ventral tegmental area, G-proteins mediate progesterone's actions at dopamine type 1 receptors for lordosis of rats and hamsters.

RATIONALE: Previous reports indicate that the ventral tegmental area (VTA) and/or progesterone (P) can modulate the reinforcing effects of drugs of abuse, food, and sexual behavior. OBJECTIVES: We investigated if, in the VTA, P's membrane-mediated actions for lordosis involve dopamine type 1 receptors (D(1)). Also, whether P's actions at D(1) for lordosis are mediated by typical G-protein coupled mechanisms was examined. METHODS: In Exps 1 and 2, rats received estradiol (E(2) 10 microg) at h 0 and infusions of the D(1) antagonist SCH23390 (100 ng), the D(1) agonist SKF38393 (100 ng), or vehicle, to the VTA, at h 44. Thirty minutes later, rats received systemic P (0, 50, 100, or 200 microg). Subjects were tested for lordosis and motor behavior 2.5 h later. In Exps 3 and 4, E(2)+P (rats 0 or 100 microg; hamsters 200 microg)-primed animals were pretested for lordosis and motor behavior at h 47.5 and infused with SKF38393 (100 ng) or vehicle to the VTA. Thirty minutes later, subjects were retested and infused with the G-protein inhibitor guanosine 5'-O-(2-Thiodiphosphate) (GDP-beta-S; 50 microM) or vehicle. Post-testing occurred 30 min later. RESULTS: Pretreatment with SCH23390-reduced and SKF38393-enhanced P's actions, in the VTA, for lordosis of E(2)-primed rats and hamsters. As well, D(1)-mediated increases in P-facilitated lordosis of rats and hamsters were inhibited by GDP-beta-S. Changes in lordosis were independent of large alterations in motor behavior. CONCLUSIONS: In the VTA, P has actions for modulating reinforcing behaviors, such as lordosis, at D(1) that are G-protein-mediated.

2,3,4,5-Tetrahydro-7,8-dihydroxy-1-phenyl-1H-3-ben↗

Epidemiology of low back pain in the elderly: correlation with lumbar lordosis.

We carried out an epidemiologic study to determine the prevalence of low back pain in elderly Japanese and to examine the correlation with lumbar lordosis in sagittal plane radiographs. Low back pain is an enormous clinical and public health problem. With the increasing use of spinal instrumentation, the measurement of lumbar lordosis is thought to be important. However, in elderly Japanese, the prevalence of low back pain and its correlation with lumbar lordosis is not clear. Five hundred and nine people, aged 50-85 years, were examined, and 489 subjects met our criteria. Clinical findings, physical status, and the visual analogue scale (VAS) of pain were examined in these subjects. Measurements and determination of total lordosis from L1-S1 were made from standing radiographs. Forty-eight percent of the subjects had experienced low back pain within the previous 3 months. Women had low back pain more frequently (P = 0.006). There was a significant difference in lumbar lordosis between the groups with and without low back pain (P = 0.0006). Lumbar lordosis was approximately 4 degrees less in the low back pain group and there was no relationship to age or sex in either group. VAS was significantly inversely correlated with lumbar lordosis (P = 0.025, at rest). The body mass index (BMI) of the low back pain group was higher in women, but the difference was not significant (P = 0.06). In conclusion, lumbar lordosis was defined and its prevalence in elderly Japanese was reported together with VAS and physical data used to compare the two groups.

Aged↗

Bilateral implantation of low-profile interbody fusion cages: subsidence, lordosis, and fusion analysis.

BACKGROUND CONTEXT: The use of interbody fusion cages as a treatment for degenerative disc disease has become widespread. Low-profile cages have been developed to allow a closer fit when implanting bilateral cages in patients with smaller vertebral bodies. Some surgeons feel the open design also allows better bone contact and visualization. This is particularly true when two low-profile cages are used adjacent to one another. Because of the open design of low-profile interbody fusion cages, there has been concern regarding such issues as subsidence, lordosis and fusion rates. PURPOSE: This retrospective review of paired bilateral reduced profile interbody fusion cages was completed to assess changes in subsidence, lordosis and fusion. As a secondary goal, patient outcomes were measured to determine overall health since surgery and the patient's satisfaction with the spine surgery, in an attempt to assess the effect of the outcome variables cited supra. STUDY DESIGN: This was a retrospective evaluation of patients who underwent anterior lumbar interbody fusion with low-profile interbody fusion cages. PATIENT SAMPLE: Seventy-one consecutive patients who underwent bilateral implantation of low-profile interbody fusion cages were evaluated. OUTCOME MEASURES: A patient self-evaluation, which included a Short Form (SF)-36 and questions regarding patient satisfaction were administered to patients who were at least 1 year postoperative. Subsidence and lordosis measurements were completed. Fusion was assessed by the operating surgeon. METHODS: Low-profile interbody fusion cages (BAK/Proximity, Centerpulse Spine-Tech, Inc., Minneapolis, MN) were implanted bilaterally in at least one level from L3-L4 to L5-S1. Most patients had degenerative disc disease with leg and back pain that was not responsive to conservative treatment and demonstrated segmental instability or collapse. A small percentage of patients had either a degenerative spondylolisthesis (7.0%) or an isthmic spondylolisthesis (4.2%). Autograft harvested from the iliac crest was used in all cases. Demographic, surgical and follow-up data were retrospectively collected from patient charts. A clinical outcome questionnaire that included an SF-36 as well as questions regarding patient satisfaction was either mailed to each patient who was at least 1 year postsurgery or given to patients to complete at their 1-year visit. Patients were routinely followed radiographically before surgery, immediately after surgery and at 3, 6, 12 and 24 months after surgery. Fusion was assessed by the operating surgeon using lateral radiographs often in conjunction with a thin-slice computed tomography (CT) scan. Criteria for a successful fusion were lack of motion, anterior bridging bone and lack of lucencies on flexion/extension X-rays and/or contiguous bone through the cage using a thin-cut sagittal CT scan. Lateral X-rays on each patient were also measured for subsidence and lordosis changes. RESULTS: A total of 71 patients (45 men, 26 women) with a mean age of 43.4 years (range, 25 to 74) were evaluated. Thirty-six percent of the patients were smokers, and 96% were worker's compensation patients. Thirty-two percent of the patients had previous lumbar surgery. A total of 100 operative levels were evaluated. There were 45 one-level, 23 two-level and three three-level cases. Forty-nine percent were level L5-S1, 43% were L4-L5 and 8% were L3-L4. The mean duration of symptoms was 31.5 months. Mean surgical time, mean blood loss and mean hospital stay were 139 minutes, 186 cc and 3.34 days, respectively. There were no intraoperative or postoperative complications attributable to the construct and no cases of cage migration or collapse. Patients who were at least 1-year postsurgery and had follow-up X-rays or had undergone a CT scan at this time point were evaluated for fusion status. Sixty-three patients were assessed for fusion. Fifty-four (86%) of these patients were determined to have a solid fusion. Mean time to fusion was 10 months. Fusion was assessed as solid only if all operative levels were fully fused. Mean subsidence of the anterior region was 1.97 mm, whereas the mean subsidence of the posterior region was 0.82 mm. Lordosis was unchanged at all surgical levels with mean lordosis in L3-L4 decreasing only slightly from 13 degrees before surgery to 12 degrees after surgery. L4-L5 and L5-S1 showed only slight increases in lordosis changing from 17 to 18 degrees at L4-L5 and from 17 to 19 degrees at L5-S1. These changes were not statistically significant. The clinical outcome questionnaires had a return rate of 68%. Of the 48 patients who completed the questionnaire, 75% responded that they were happy with the surgical results and would definitely recommend the surgery to a friend. Sixty-seven percent agreed that surgery met their expectations or that surgery improved their condition enough that they would go through it again for the same outcome. The results of the SF-36 portion of the survey revealed that the physical and mental composite scores were within normal range of the US population that has experienced back pain or sciatica. CONCLUSION: Bilateral implantation of low-profile cages in this patient population led to satisfactory outcomes. Subsidence and changes in lordosis were minimal. Fusion rates were good, especially for one-level cases. Patient satisfaction was relatively high, considering the population consisted of 96% worker's compensation cases. With proper surgical technique, bilateral low-profile cages can be used effectively to treat patients with degenerative disc disease.

Health Status↗

Hypothalamic grafts induce the recovery of lordosis in female hamsters with lesions of the ventromedial hypothalamus.

Previous studies have documented the ability of neural grafts to stimulate the recovery of lordosis from neurochemical deficits. However, it was unclear if grafts also could reverse deficits in lordosis caused by lesions at critical points in the neural circuit controlling this response. To address this question, female hamsters were subjected to unilateral lesions of the ventromedial hypothalamus (VMN), a structure well known for its mediation of hormonal effects on lordosis. The effects of these lesions were described by noting the ability of manual stimulation of one flank to reinstate a deteriorating lordosis response. Consistent with past results, unilateral VMN lesions decreased responsiveness to stimulation of just the contralateral flank. Females showing such lateralized decrements then received control treatments or implants into the lesioned area of basal hypothalamic tissue from a neonatal male or female hamster. Approximately 1 month later, tests of lordosis reinstatement by ipsi- or contralateral manual stimuli were repeated. Whereas lateralized decrements in responsiveness persisted in control subjects, implants of tissue from male or female neonates led to reliable improvements in lordosis, reversing the lesion-induced decrease in contralateral responsiveness. The mechanism responsible for this change is unclear, but could involve an elevation in a lordosis-facilitating neuromodulator. Alternatively, it could depend on the reinforcement or replacement of neural circuits for lordosis, possibly including those that connect the two VMNs with each other or with the periaqueductal gray of the midbrain.

Animals↗

Regulation of estrogen-stimulated lordosis behavior and hypothalamic progestin receptor induction by antiestrogens in female rats.

Two estrogen antagonists, CI-628 (CI) and tamoxifen (TX), were used to examine the relationship between estrogen priming of lordosis behavior and progestin receptor induction in the hypothalamus-preoptic area (HPOA) of ovariectomized female rats. Lordosis behavior was assessed by measuring lordosis quotients (LQ) in response to injection of 2 micrograms of estradiol benzoate (EB) followed 48 hr later by 500 micrograms of progesterone (P). Behavior testing began 4 hr after P injection. The effects of antiestrogens were assessed by injecting CI and TX (1-2 mg) from 0 to 48 hr prior to EB. Levels of cytosol progestin receptor in the HPOA were determined by quantifying the specific binding of 0.5 nM [3H]R5020 to cytosols from animals receiving the same EB and antiestrogen treatments used in behavioral testing. TX given concurrently with or CI given 2 hr before EB abolished both lordosis behavior and induction of HPOA progestin receptors. In contrast, CI given 12 hr prior to EB abolished lordosis but permitted a 95% elevation in the concentration of progestin binding sites in the HPOA. TX or CI given 48 hr before EB resulted in moderate levels of lordosis (mean LQs from 56 to 69) and induction of HPOA progestin receptors from 85 to 130% above noninjected controls. However, CI given 24 hr prior to EB produced less than a 40% increase in brain R5020 binding even though lordosis behavior was equivalent to that seen in the 48-hr animals (mean LQ = 53). These data indicate that the effects of antiestrogens on female sexual behavior and on the synthesis of brain progestin receptors depend on which antiestrogen is used and the time interval between administration of estrogen and antiestrogen. They also demonstrate that under some conditions estrogen induction of cytosol progestin receptors in the HPOA can be dissociated from estrogen priming of lordosis behavior in rats.

Animals↗

Estrogen but not progesterone facilitates the lordosis reaction to cervicovaginal stimulation of ovariectomized rats.

Ovariectomized rats were treated sequentially with 1, 10 or 100 micrograms/kg of estradiol benzoate and 8 mg/kg of progesterone (or vehicles) and were tested for lordosis reactivity. A male was used to apply cutaneous stimulation only, or cutaneous and cervicovaginal stimulation, in females with masked or unmasked vaginal orifices, respectively. Graded cervicovaginal stimulation alone was obtained with a manually operated penile dummy. Progesterone caused a significant increase in the lordosis quotient to male stimulation after the doses of 10 and 100 micrograms/kg of estrogen but not after 1 microgram/kg of the hormone. This effect of progesterone was unaffected when the vaginal orifice was masked to avoid penile intromission and the resulting cervicovaginal stimulation. Lordosis reactions to artificially graded cervicovaginal stimulation following progesterone only or vehicle only were both infrequent and weak. The three estrogen doses employed increased markedly the reactivity to cervicovaginal stimulation, both when the percent frequency of lordosis and when lordosis intensity ratings were considered. In contraposition with the effect on male stimulation, progesterone did not increase the reactivity to cervicovaginal stimulation, as measured by the percent incidence of lordosis. This was also the case when lordosis intensity scores were considered, with the sole exception of a significant difference when 1 microgram/kg of estradiol and the strongest stimulation were used. Our results suggest that the sensitivity of the afferent pathways to elicit the lordosis reaction are under different hormonal modulations: cutaneous afferents seem to be facilitated by estrogen and progesterone, while cervicovaginal afferents would be facilitated only by estrogen.

Animals↗

Cholecystokinin stimulates and inhibits lordosis behavior in female rats.

Recently, IP CCK-8 has been shown to inhibit lordosis in sexually experienced, estradiol benzoate (EB) and progesterone (P) primed rats. However, receptivity is influenced by prior sexual experience and/or exposure to sex steroids, as well as the steroid dosage administered before testing. Thus, we examined the effect of CCK-8 (3 micrograms/kg; IP) on lordosis in rats with different degrees of receptivity. Three weeks after ovariectomy, females were treated with EB followed 48 hr later with P, or with EB alone. CCK-8 significantly facilitated lordosis in rats given 5 micrograms EB. Following a 5 week nonexperimental period, animals were more receptive and CCK-8 significantly inhibited lordosis in the 5 or 10 micrograms EB groups. In a separate experiment, rats were ovariectomized, adrenalectomized, and treated with EB alone. As in the first experiment, CCK-8 facilitated and inhibited lordosis. CCK-8's effects were highly dependent on the female's receptivity, facilitating lordosis when receptivity was low and inhibiting lordosis when receptivity was high (but not maximal). In conclusion, IP CCK-8 modulates lordosis behavior independent of P, but its effects depend on the female's degree of receptivity.

Adrenalectomy↗

Effect of subcutaneous vs intraperitoneal administration of an anti-estrogen, CI-628, estradiol-and estradiol benzoate-stimulated lordosis in the ovariectomized rat.

The anti-estrogen CI-628 (3 mg) inhibited estradiol (E, 150 mug, SC in oil)-stimulated lordosis in ovariectomized rats, when the anti-estrogen was given intraperitoneally (IP) at the time of E injection (Hr 0). No lordosis inhibition occurred after similar treatment, if the CI-628 was given subcutaneously. For estradiol benzoate (EB, 2 mug, SC in oil)-stimulated lordosis, CI-628 (Hr 0) had a substantial inhibitory effect whether it was given IP or SC, the greater percentage inhibition occurring after SC CI-628 (Experiment 1). All animals received sequential injections of estrogen and progesterone (500 = s,g, SC in oil) and were then tested to 10 mounts by an intact male. These results suggested that, after E injection, neural tissues mediating lordosis have a shorter period of sensitivity to the behavioral effects of CI-628 than after EB injection. Thus, inhibition of E-stimulated lordosis apparently required the more rapid onset of intracellular estrogen retention inhibition resulting from CI-628 given IP rather than SC. This was not the case for EB-stimulated lordosis, where a longer period of sensitivity to CI-628 seeemed likely. This hypothesis was supported by the data of Experiment 2, in which CI-628 (3 mg, IP) was first given 3 hr after E or EB treatment. In this paradigm, CI-628 no longer inhibited E-stimulated lordosis. In contrast, the anti-estrogen's effect on EB-stimulated lordosis was at least equal to the inhibition occurring after CI-628 (IP) given at Hr 0.

Animals↗