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PubMed1980

Suppression of sexual receptivity in the female hamster: neuroanatomical projections from preoptic and anterior hypothalamic electrode sites.

Electrical stimulation (ES) through fine-wire electrodes chronically implanted in the preoptic area and anterior hypothalamus suppressed the lordosis response in freely moving hormone-primed female hamsters. ES at these sites never induced or facilitated lordosis. When behavioral testing was completed small lesions were made at the tips of the electrodes, and the Fink-Heimer method was used to trace degenerating axons away from the sites of ES. This was done in an effort to determine the neural pathways important for the modulation of this behavior. The hypothalamic distribution of the stria terminalis was also charted for the hamster and was found to be similar to that in the rat, including projections to both the shell and core of the ventromedial nucleus (VMN). No single pattern of degeneration was common to all females showing ES-produced lordosis suppression. These data demonstrate that stimulation of several different pathways can produce behavioral states that are incompatible with the lordosis response. We suggest that ES in the medial preoptic-medial anterior hypothalamic continuum suppresses sexual receptivity by influencing neurons in the VMN region, while ES through more laterally placed electrodes suppresses receptivity by producing an incompatible state of behavioral activation, without directly influencing VMN region neural activity.

Amygdala↗
PubMed1980

Hormone-induced enlargement of receptive fields in trigeminal mechanoreceptive neurons. I. Time course, hormone, sex and modality specificity.

The phenomenon of hormone induced enlargement of receptive field area in mechanoreceptive neurons was investigated with respect to time course, hormone, sex and modality specificity. In acute recording experiments, threshold receptive field boundaries of single trigeminal ganglion neurons innervating the facial region of rats were determined for several different treatment groups. Among ovariectomized females injected with estradiol benzoate (EB) for 2, 5 or 10 days, receptive field areas were significantly increased after only 2 days. Enlargement of field areas appeared to be maximal after 5 days of EB. Lordosis behavior was observed after 10 days of EB but not after 2 or 5 days, suggesting that receptive field enlargement occurs independently of hormone induced lordosis behavior. In normal, intact females, receptive field area varied significantly with the estrous cycle (large during estrus, small during diestrus) indicating that this phenomenon is naturally occurring, not dependent upon the method of estrogen administration. Progesterone given for 10 days had no effect on receptive field area. Treatment with 2 days of EB followed by a single progesterone injection produced reliable lordosis but did not result in any further increase in receptive field area beyond the increase produced by 2 days of EB alone. Thus the synergism between estrogen and progesterone that is recognized for induction of lordosis is absent with respect to receptive field enlargement. The small increase in field area following 10 days of testosterone treatment could be accounted for by the fact that such animals, had blood serum estradiol levels comparable to animals given 2 or 5 days of EB, possibly the result of a testosterone to estrogen conversion. It was concluded that hormone induced receptive field enlargement appears specific for estrogen. Castrated male rats treated with 10 days of EB show the same increase in receptive field area as females, indicating that the phenomenon is not specific to females. Analysis of receptive field area as a function of receptive field type and adaptation rate showed that EB induced field area enlargement was specific to rapidly adapting mechanoreceptive neurons.

Animals↗
PubMed1983

Estrogenic maintenance of lordotic responsiveness: requirement for hypothalamic action potentials.

Studies were conducted to determine the requirement for hypothalamic, sodium current-based action potentials in the performance of a stereotypic, estrogen-dependent reflex, the lordosis response. Intrahypothalamic infusion of local anesthetics (50% procaine or 0.5% bupivacaine) into conscious rats had no effect on lordotic responsiveness, and, in a separate group of urethane-anesthetized rats, depressed multiunit electrical activity temporarily. Intrahypothalamic infusion of tetrodotoxin into conscious rats, however, resulted in a dose-dependent, reversible decline in lordotic responsiveness. The first significant drop in lordotic responsiveness occurred 40 min after infusion; the minimum was reached 2-4 h after infusion. Recovery of lordotic responsiveness to preinfusion levels was complete by 12-24 h after infusion. Electrophysiological studies in a separate group of urethane-anesthetized rats revealed that intrahypothalamic tetrodotoxin infusion in most cases suppressed multiunit activity completely usually within 6 min, and this suppression lasted for at least several hours. These data indicate that large, prolonged decreases in electrical activity in the hypothalamus, where estrogenic action is necessary and sufficient to induce lordosis, result in a gradual, reversible decline in lordotic responsiveness. These data are consistent with a 'tonic' rather than a 'mount-by-mount' role of hypothalamic neurons in lordosis. Furthermore, since lordotic responsiveness declined only when hypothalamic electrical activity had been disrupted severely for at least 40 min, it is postulated that the neuroactive products released by lordosis-relevant, hypothalamic neurons may have a duration of action of at least several minutes.

Action Potentials↗
PubMed1985

Increased estrogen receptor binding in amygdala correlates with facilitation of feminine sexual behavior induced by olfactory bulbectomy.

In this experiment we tested the hypothesis that the potentiation of feminine sexual behavior following olfactory bulb removal in female rats would be associated with increased ovarian steroid receptor binding in brain. Ovariectomized adult female rats underwent either bilateral olfactory bulb removal (BOB) or a sham operation and were exposed to 100% estradiol (E2) in silastic capsules for 4 or 6 h. Following behavior testing, either cell nuclear estrogen receptor levels were measured in amygdala, hypothalamus, preoptic area and pituitary, or cytosol progestin receptors levels were determined in cortex, preoptic area and hypothalamus. After 6 h E2 exposure, BOB females showed increasing lordosis responding with increasing progesterone (P) doses, at levels significantly higher than those of sham-operated rats. After 4 h E2 exposure bulbectomized rats showed both a facilitation of lordosis and elevated estrogen receptor levels in amygdala. Sham-operates showed neither response to the 4 h E2 stimulus. For both BOB and sham groups, progestin receptors were induced after 6 h E2 exposure, but were uninduced after 4 h E2 exposure. Additional rats were exposed to 5% E2 for 24 or 48 h, followed by P. Lordosis was potentiated in BOB rats at 24 h; sham-operates showed high levels of lordosis only after 48 h of 5% E2 exposure. Proceptivity was enhanced in BOB rats after both 24 and 48 h of 5% E2 exposure. In contrast, proceptivity was rarely observed in sham-operates, or in either group after 4 or 6 h E2 exposure. We propose that increased estrogen receptor binding in the amygdala may provide a biochemical basis for the increased estrogen sensitivity found in olfactory bulbectomized female rats.

Amygdala↗
PubMed1985

Intrahypothalamic infusions of a synthetic heroin substitute, N-methyl-4-phenyl-1,2,3,6-tetrahydropyridine, potentiate mating behaviour in the female rat.

Acute microinfusions of N-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) bilaterally into the arcuate-ventromedial area of the hypothalamus (ARC-VMH) produced a dose-dependent facilitation of lordosis behaviour in oestrogen- and oestrogen-progesterone-treated ovariectomized female rats. This facilitation could be blocked by pretreatment of the ARC-VMH site with pargyline but not by a potent antagonist analogue of gonadotropin releasing hormone (GnRH). MPTP was not effective in potentiating lordosis when microinfused into other brain sites which are intimately involved in the neural circuitry for this oestrogen-dependent behavioural response. This action of MPTP in the ARC-VMH may be dependent upon the high MPTP receptor densities which are known to occur in the arcuate and periventricular hypothalamic nuclei. Chronic infusions of MPTP (once daily for 21 days) into the ARC-VMH did not result in any significant cell loss and did not interfere with the ability of a later acute MPTP infusion to potentiate lordosis nor with the ability of oestrogen and progesterone to promote the full display of lordosis behaviour. These results provide the first demonstration of neurally placed MPTP in the regulation of a specific hormone-dependent neuroendocrine response.

1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine↗
PubMed1986

Regulation of mating behaviour in the female rat by gonadotropin-releasing hormone in the ventral tegmental area: effects of selective destruction of the A10 dopamine neurones.

Microinfusions of gonadotropin-releasing hormone (GnRH) into the ventral tegmental area (VTA) potentiated lordosis behaviour in oestrogen-primed ovariectomised female rats. Facilitation was observed within 5 min after the infusion and lasted for about 90 min. When GnRH was infused into the VTA of oestrogen-primed animals which were previously subjected to 6-hydroxydopamine treatment (to destroy the A10 dopamine cells), it produced a marked facilitation of lordosis lasting for about 24 h. These results suggest that the A10 dopamine neurones in the VTA may be critically involved in the mechanisms by which GnRH may modulate midbrain circuits involved in the regulation of lordosis behaviour in the female rat. The lesion studies also imply that the A10 dopamine neurones function as inhibitory neurones regulating lordosis behaviour by suppressing the activity of those cells in the VTA which are sensitive to GnRH. Removal of this inhibitory input leads to an exaggerated response.

Animals↗
PubMed1993

Female sexual behavior following intracerebral infusion of the 5-HT1A agonist, 8-OH-DPAT, into the medial preoptic area.

The effects of intracerebral infusions of the 5-HT1A agonist, 8-hydroxy-2-(di-n-propylamino)tetralin (8-OH-DPAT), on sexual behaviors of intact, proestrous rats were examined. When administered into either the rostral or the caudal portions of the medial preoptic area (mPOA), bilateral infusions of 200, 500, or 2,000 ng of 8-OH-DPAT reduced lordosis behavior (e.g. the lordosis/mount ratio; L/M) and increased the female's resistance to the male's attempts to mount. Infusions within the mid-rostrocaudal mPOA failed to suppress lordosis behavior but were as effective as the rostral or caudal infusions in the elicitation of resistive behavior. A reduction in the L/M ratio was usually accompanied by a slight decline in the quality of the lordosis reflex; proceptivity, as evidenced by the occurrence of hopping and darting behavior, was not consistently reduced by 8-OH-DPAT. In fact, 4 out of 7 rats that received mid-rostrocaudal infusions of 8-OH-DPAT showed a "frenzied" accentuation of hopping and darting behavior. These results suggest that 5-HT1A receptors in the mPOA play an important role in several components of female sexual behavior. The identification of a rostral and caudal location of mPOA sites where 8-OH-DPAT suppressed lordosis behavior is consistent with the organization of 5-HT fibers in the mPOA and with ventromedial hypothalamic (VMN) input into the mPOA.

8-Hydroxy-2-(di-n-propylamino)tetralin↗
PubMed1996

The medullary reticular formation is a site of muscle relaxant action of diazepam on deep back and neck muscles in the female rat.

We tested the hypothesis that the effect of systemic injections of diazepam (DZ, 125 mg/kg) to reduce the quality of the reproductive behavior, lordosis, and to reduce the EMG of lumbar back muscles involved in lordosis (Schwartz-Giblin et al., 1984) is exerted through a reticulospinal pathway with cells of origin in the nucleus gigantocellularis that excites lumbar motoneurons indirectly (Robbins et al., 1990, Robbins et al., 1992). In contrast, DZ facilitates lordosis behavior when infused into the midbrain central gray (McCarthy et al., 1995). Direct deposits of crystalline mixtures of DZ (20-80 ng) in dextrose were delivered to the medullary reticular formation (MRF) by diffusion from a cannula inserted through a guide to which a bipolar stimulating electrode was attached. The multiunit EMG response evoked by 20 (300 ms long) stimulus trains was recorded in back and neck muscles, lateral longissimus and splenius before and 5, 15, 30 and 60 min after local DZ deposits. There was a significant reduction in EMG response over this time period when stimulus intensities were within the range of 1.2-1.5 times threshold (Friedman two-way non-parametric test, P < 0.002). Large amplitude motor units that provide large tensions were the most sensitive to DZ-induced inhibition. Control deposits of dextrose had no significant effect. Systemic injections of progesterone (1 mg, i.p.) 60 min after DZ deposits, but not after dextrose deposits, further reduced the MRF-evoked EMG responses over the course of 1 h. As predicted, DZ infusions into the midbrain central gray did not reduce the reticulospinal-evoked axial muscle response, consistent with the facilitatory effect of midbrain central gray infusions of DZ on the lordosis quotient. The results suggest that benzodiazepine agonists (if endogenous) acting at sites in the MRF would be effective muscle relaxants during pregnancy, prior to the fall in progesterone that precedes labor.

Animals↗
PubMed1983

Inhibition of estrogen-activated sexual behavior by androgens.

Experiments to determine the potential of androgen to inhibit estrogen-activated female sexual behavior in rats were conducted. Treatment with either testosterone propionate (0.8 or 1.6 mg/day) or dihydrotestosterone propionate (0.2, 0.4, or 0.8 mg/day) significantly reduced the incidence of lordosis in ovariectomized females receiving estradiol benzoate (1 microgram/day). A similar suppression of estrogen-activated lordosis by testosterone was observed in castrated male rats. Flutamide, an androgen-receptor blocker, prevented the inhibition of lordosis by testosterone in females, indicating that the interaction of testosterone or a metabolite with an androgen receptor may be an important feature of this inhibition. Furthermore, the ability of dihydrotestosterone to inhibit lordosis at lower doses than testosterone suggests that the conversion of testosterone to dihydrotestosterone may also be necessary. These experiments demonstrate the potential of testosterone to inhibit the occurrence of female sexual behavior in rats, in contrast to its established facilitative effect on this behavior.

Androgens↗
PubMed1987

Selectivity in the responses of hamsters to conspecific vocalizations.

Lordosis responses by estrous hamsters were triggered by brief manual stimulation. Lordosis durations then were timed, as manual stimulation was discontinued, and subjects were exposed to tape-recordings of conspecific vocalizations reproduced at intensities of 0-60 dB SPL. Relative to the durations observed in the presence of ambient noise alone, recordings of stress-elicited screams failed to facilitate lordosis regardless of stimulus intensity. In contrast, ultrasounds by male or female hamsters did prolong lordosis, and to extents that were directly related to intensity but unrelated to the sex of the caller. The very different responses to screams and ultrasounds suggest that the ability to facilitate sexual behavior is at least somewhat specific to ultrasounds and is not shared by all vocalizations reflecting states of high general arousal. On the other hand, the similar responses elicited by male and female ultrasounds suggest that these calls convey similar messages and that structural differences between them effect changes in call localizability, not meaning.

Acoustic Stimulation↗
PubMed1987

Male stimuli are necessary for female sexual behavior and uterine growth in prairie voles (Microtus ochrogaster).

In reproductively naive female prairie voles (Microtus ochrogaster) direct contact with male urine or housing in a male-soiled cage, in the absence of physical contact, resulted in increased uterine weights, but did not reliably elicit behavioral estrus (defined by lordosis). Physical contact with an unfamiliar male, for 1 hr or more, followed by 30 or 48 hr of continuous access to a male-soiled cage, induced lordosis in approximately two-thirds of the females tested. When females were physically exposed to a male for 18 hr and tested 6 hr later, 70% showed lordosis. However, when females receiving either 1 or 18 hr of male contact were removed from the presence of the male and placed in a clean cage for 24 hr, only 29-37% of the females subsequently showed lordosis. These results suggest that direct physical contact with the male or chemical stimuli from the male may be necessary to induce and maintain behavioral estrus in female prairie voles.

Animals↗
PubMed1989

Reversal of androgen inhibition of estrogen-activated sexual behavior by cholinergic agents.

Androgens have been found to inhibit lordosis activated by estrogen treatment of ovariectomized female rats. In the present experiments, dihydrotestosterone propionate (200 micrograms for 3 days) inhibited the incidence of lordosis in ovariectomized females treated with estradiol benzoate (1 microgram for 3 days). This inhibition of lordosis was reversed 15 min after bilateral intraventricular infusion of physostigmine (10 micrograms/cannula), an acetylcholinesterase inhibitor, or carbachol (0.5 microgram/cannula), a cholinergic receptor agonist. This reversal of inhibition appears to be mediated by cholinergic muscarinic receptors since pretreatment with scopolamine (4 mg/kg, ip), a muscarinic receptor blocker, prevented the reversal of androgen inhibition by physostigmine. These results indicate that androgens may inhibit estrogen-activated lordosis through interference with central cholinergic muscarinic mechanisms.

Animals↗
PubMed1996

Rogers' posterior cervical fusion--a 3-month radiological review.

Rogers described his technique of spinal fusion in 1942, and since then numerous other techniques have been described but no large series describing the anatomical results has been reported. To assess the technical success of Rogers' technique, to identify factors that contribute to less than ideal anatomical results, and to suggest methods of avoiding potential pitfalls, the anatomical results of Rogers' posterior cervical fusion were compared with what we consider an ideal anatomical result by analysis of the 12-week post-operative flexion/extension radiographs. One hundred and sixty-one Rogers-type posterior cervical fusions using either wire or Ethibond were performed for flexion injuries. The 12-week post-operative flexion extension radiographs were assessed for union, fusion of extra levels, residual kyphosis/listhesis, excessive lordosis, and hypermobility. Results were related to the presence of associated fractures, using the chi 2 test. Bony union was seen in 100 per cent of cases. Fusion of additional levels occurred in 40 (25 per cent), residual kyphosis in 54 (34 per cent), listhesis in 14 (9 per cent), and excessive lordosis in seven (4 per cent). Hypermobility at the adjacent level occurred in 10 (6 per cent), and at a distant level in five (3 per cent). Statistically significant associations occurred between fusion of extra levels and fractures, residual kyphosis and fractures, excessive lordosis with the use of wire rather than Ethibond, and the desired anatomical result with absence of fracture. The Rogers technique is a safe, easy and reliable method of achieving cervical fusion, with a 100 per cent fusion rate at 3 months in this series. However, the intended position of fusion, between 1 degree-5 degrees of lordosis, with normal alignment, is not always achieved. There is also a high incidence of fusion of levels other than those intended. We believe that the incidence of these problems could be reduced by more attention to surgical detail.

Adolescent↗
PubMed1989

Changes in estrogen receptors in the mediobasal hypothalamus mediate the facilitory effects exerted by the male's olfactory cues and progesterone on feminine behavior in the male rat.

The purpose of this study was to determine whether facilitory effects exerted by olfactory cues on lordosis behavior in the male rat involved changes in estradiol receptors at the hypothalamic level. Male rats were orchidectomized as adults. They were given either 25 micrograms estradiol benzoate (EB) alone or 25 micrograms EB and 100 micrograms progesterone (P) sequentially and exposed or not to the odor of male urine. Some of them were tested for lordosis behavior at 8 h after P. The other ones were killed 4 h after P and used for estradiol (E2) and P receptor assay in mediobasal hypothalamus (MBH). Olfactory cues were shown to increase the number of E2 receptors in both the animals given EB or EB + P. Progesterone as such appeared to be capable of increasing the number and the rate of occupancy of E2 receptors. A population of constitutive and estrogen-inducible P receptors was detected in the MBH. Since only the animals given EB + P were shown to be sensible to the facilitory effects of male urine on lordosis behavior, it may be assumed that E2 and P on one hand and olfactory cues on the other exert cumulative effects at the level of the MBH and that both a high level and a high rate of occupancy of E2 receptors are necessary for the olfactory cues to facilitate the display of lordosis behavior in the male rat.

Animals↗
PubMed1982

Changes in estrogen and progestin receptor binding resulting from retrochiasmatic knife cuts.

Retrochiasmatic frontolateral knife cuts (FLC) or sham operations (Sham) were performed with a Halasz-type knife. All animals were primed with estrogen plus 0.5 mg progesterone (P) and tested for lordosis both before and after surgery. Two weeks after the last test they received estradiol (E2) in Silastic capsules and were sacrificed 2 days later for determination of either nuclear estrogen receptors or cytosol progestin receptor binding in brain and pituitary (PIT). Rats which had received FLC showed significantly lower lordosis quotients relative to Shams, and relative to their own pre-surgery scores. Nuclear E2-receptor binding was significantly reduced in the hypothalamus (HYPO) following FLC, but not in preoptic area (POA) or PIT. No changes in cytosol P-receptor binding were observed in HYPO, POA or PIT following FLC. Our results suggest a positive correlation between the number of hypothalamic E2-receptors and the capacity to display lordosis, and emphasize the importance of anterolateral connections to the HYPO for the progesterone-induced facilitation of lordosis.

Animals↗
PubMed1986

Sexual behavior in the female rat following removal of the vomeronasal organ.

We used female Wistar rats from which the vomeronasal organ (VNO) has been removed. The first question addressed was whether such females would show deficits in sexual behavior. The data left no doubt that removal of the VNO severely depressed lordosis as well as such proceptive behaviors as "darting" and "hopping." We then injected estrogen and progesterone and, in still another experiment, estrogen and luteinizing hormone-releasing hormone (LHRH). Estrogen and progesterone significantly enhanced lordosis, but only estrogen and LHRH raised the lordosis quotient of VNO-ablated females to that of the control females. We discuss the results in terms of a theoretical model involving the complementary action of estrogen and LHRH in inducing lordosis in the intact female.

Animals↗
PubMed1986

REM sleep deprivation facilitates the estrogen effect on heterotypical sexual behavior in male rats.

Gonadectomized male rats were submitted to REM sleep deprivation (REMd) for 120 hr and their hetero and homotypical sexual response to estradiol benzoate (EB) was tested. Subjects (Ss) receiving 20 micrograms EB showed lordosis quotients (LQ) twice as high as those receiving 10 micrograms EB and at the same time the LQs in these groups were higher than in the non-REMd groups. Gonadectomized-adrenalectomized control Ss showed the highest levels of lordosis throughout the experiment. REMd by itself does not produce lordosis response. The results indicate that the brain structures underlying this behavior in males are probably similar to those in females, since REMd increases lordosis in both cases. The lack of homotypical sexual behavior normally observed in gonadectomized male rats does not seem to be affected by this treatment. The issue of adequate controls for REMd experiments is discussed.

Animals↗
PubMed1990

Hypothalamic effects on medullary reticular activation of deep back muscle EMG.

Medullary reticular stimulation can activate deep back muscle EMG in urethane-anesthetized female rats. Midbrain central gray stimulation can facilitate brainstem reticular control over deep back muscles. Since these deep back muscles lateral longissimus (LL) and medial longissimus (ML) execute the vertebral dorsiflexion of lordosis behavior, and since the motor control hierarchy sketched above parallels lordosis behavior circuitry, we tested the hypothesis that medial hypothalamic lesions (which, in behavioral experiments, decrease lordosis) can also reduce medullary reticular activation of deep back muscle EMG. Urethane-anesthetized rats were tested systematically for amplitude of lateral longissimus (LL) and medial longissimus (ML) EMG responses to electrical stimulus trains applied to the nucleus gigantocellularis (NGC) of the medullary reticular formation, before and after electrolytic lesions of the ventromedial hypothalamus (n = 18) or control sites (n = 30). Bilateral ventromedial hypothalamic lesions were able to greatly reduce EMG responses in LL and ML, often with a time course similar to previous lordosis behavioral results. Surprisingly, lesions at the anterior ventromedial nucleus pole were particularly effective, and may reflect importance of intraventromedial local neurons. Although, on the average, various control lesions were less effective, the ventromedial hypothalamic effect was not unique. For example, it was possible to see an EMG decrease following lesions of the dorsomedial thalamus. Nevertheless, EMG loss was not well correlated with changes in the cortical EEG, and thus does not appear to be a simple consequence of changes in "arousal." In conclusion, it appears that ventromedial hypothalamic neurons can affect medullary reticular control of back muscle EMG, but must share this role with other forebrain elements.

Animals↗