Mild restraint reduces the time hormonally primed rats spend with sexually active males

The effect of 5 min of restraint on the time sexually-receptive females spend in the compartment of a sexually active male was examined. Ovariectomized females, hormonally primed with 10 microg estradiol benzoate and 500 microg progesterone (EP) or primed only with estradiol benzoate (EO) were used. After the restraint or home-cage experience, females were tested for 30 min in a chamber that allowed the female to escape to a small "burrow". Females, subjected to restraint, left the male's compartment faster and spent significantly less time in the male's compartment than did non-restrained females. This was true for both EP and EO females. When females were injected with the 5-HT(2B/2C)-receptor antagonist, SB 206553, 15 min before restraint, time spent in the male's compartment was even further reduced. However, additional studies indicated that it was the stress of the injection rather than the action of the drug that was responsible for the female's behavior. These findings are discussed in terms of their significance to the understanding of the female's reproductive response to stress and are compared to prior findings, where lordosis behavior was significantly reduced by restraint.     

Progesterone attenuates the effect of the 5-HT1A receptor agonist, 8-OH-DPAT,and of mild restraint on lordosis behavior

Ovariectomized, hormone-primed rats were used to test the hypothesis that progesterone treatment attenuated the effects of the 5-HT(1A) receptor agonist, (+/-)-8-hydroxy-2-(di-n-propylamino)tetralin (8-OH-DPAT), on female rat lordosis behavior. Based upon prior evidence that prepriming with estradiol benzoate (EB) reduced the ability of 8-OH-DPAT to inhibit lordosis behavior, rats were preprimed with 10 microg EB 7 days before a second priming with 10 microg EB followed 48 h later with 500 microg progesterone or vehicle. Independent of the presence of progesterone, prepriming with EB attenuated the lordosis-inhibiting effects of systemic treatment with 8-OH-DPAT. However, progesterone also reduced the effects of 8-OH-DPAT and this effect was also seen in females primed only once with EB. In contrast, progesterone was relatively ineffective in attenuating the effects of bilateral infusion with 8-OH-DPAT into the ventromedial nucleus of the hypothalamus (VMN). The failure of progesterone to substantially reduce the effects of VMN infusion with 8-OH-DPAT contrasts with prior studies in which estrogen's protective action against the drug did include the VMN. Thus, while both estrogen and progesterone reduce the lordosis-inhibiting effect of 8-OH-DPAT, the mechanisms responsible for the effects of the two gonadal hormones may be different. Priming with progesterone also prevented the effects of 5 min of restraint. When rats were hormonally primed with EB and oil, rats showed a transient, but significant, decline in lordosis behavior 5 and 10 min after restraint. Rats primed with EB and progesterone were unaffected by the restraint. These results are discussed in terms of their implications for the role of progesterone in altering the 5-HT(1A) receptor modulation of lordosis behavior.     

Intracranial estradiol benzoate implants and lordosis behavior of ovariectomized guinea pigs

Adult ovariectomized Hartley guinea pigs were bilaterally implanted in the ventromedial-arcuate area, caudal anterior hypothalamus, basal anterior hypothalamic-preoptic area or midbrain with stainless steel cannulae with removable inserts. At 0 h, the animals received inserts containing crystalline estradiol benzoate or cholesterol followed 36 h later by a systemic injection of 0.6 mg progesterone. Estradiol benzoate implants in the ventromedial-arcuate area facilitated estrous behavior in 79% of animals. Median characteristics of estrous behavior, classified as ‘good-excellent’, shown by these animals were latency after progesterone injection= 3h and duration= 6h. Implants of estradiol benzoate in the basal anterior hypothalamic-preoptic area resulted in display of estrous behavior in 89% of animals. The behavior shown by these animals was categorized as ‘good’ and latency= 6h and duration= 6h. Implants of estradiol benzoate in caudal anterior hypothalamus (nucleus supra-opticus diffusus) resulted in heat in 50% of animals. Heat was classified as ‘poor’ in these animals and latency= 6h and duration= 4.5h. Maximum lordosis did not vary according to brain region and was about 6 sec for all animals facilitated by intracranial estradiol benzoate. No animals displayed estrous behavior after receiving midbrain implants of estradiol benzoate. None of the cholesterol implanted animals displayed heat. The data are consistent with the concept that there are discrete estradiol-sensitive areas in the basal hypothalamus and basal anterior hypothalamic-preoptic area with a region of relatively poor sensitivity in between.     

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

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

Nerve growth factor affects defense-related behaviors, but not lordosis, in ovariectomized, estrogen-treated rats

Effects of NGF and anti-NGF on estrogen-sensitive behaviors were examined in ovariectomized, estrogen-treated rats. Intracerebroventricular (i.c.v.) administration of NGF resulted in a significant decrease in body weight. Daily treatment with low levels of estradiol resulted in a steady increase in lordosis behavior as reflected by average lordosis quotient and lordosis score. No effects of NGF or anti-NGF on lordosis behavior were detected. Estrogen treatment also resulted in a significant increase in the number of vocalizations elicited from female controls by male contact during sex behavior. NGF-treatment enhanced this effect, resulting in significantly more vocalizations elicited earlier in the course of estrogen treatment than were elicited from non-NGF-treated controls. These effects were blocked by progesterone. An increase in the number of rejections elicited by male contact during sex behavior was also observed in NGF-treated animals relative to controls. In addition, i.c.v. infusions of anti-NGF prevented the estrogen-mediated increase in elicited vocalizations, suggesting that NGF may have a physiological role in regulating this behavior. These data implicate NGF in the regulation of specific defense-related behaviors in estrogen-treated rats. Effects of NGF and anti-NGF on immunocytochemical staining for p75^NGFR- and ChAT-like immunoreactivity were also analyzed and are discussed.     

Hypothalamic progesterone implants and facilitation of lordosis behavior in estrogen-primed ovariectomized guinea pigs

Adult ovariectomized Hartley guinea pigs were bilaterally implanted in the basal hypothalamus or anterior hypothalamic-preoptic area with stainless steel cannulae with removable inserts. In experiment 1, animals received inserts containing crystalline progesterone, 17α-hydroxyprogesterone or cholesterol 36 h after subcutaneous injection of 3.3 μg estradiol benzoate. Regardless of cannula content, about 43% of animals with implants aimed at the basal hypothalamus displayed heat. Lesions or irritation associated with implants in this region may have increased behavioral responsiveness to estrogen. However, control implanted animals (17α-hydroxyprogesterone and cholesterol) tended to have shorter heat durations and more scattered facilitatory implant sites than progesterone implanted animals, suggesting that progesterone might be acting in basal hypothalamus to facilitate lordosis. Progesterone placed in basal anterior hypothalamic-preoptic area did not facilitate lordosis. Progesterone in basal hypothalamus or basal anterior hypothalamic-preoptic area did not produce inhibitory effects on behavior.In experiment 2, a revised procedure was used to control for sexual behavior resulting from estrogen treatment alone. The control procedures revealed that most of the animals with cannulae in the ventromedial-arcuate area displayed lordosis after estradiol benzoate alone. When animals not displaying estrus in response to estradiol benzoate alone were utilized for further implantation, it was clear that progesterone placed in the ventromedial-arcuate-premammillary area facilitated the expression of short latency, long duration heat. However, animals with cannulae in the basal hypothalamus, regardless of cannula content, had short maximum lordoses. No inhibitory effects of progesterone implants (in ventromedial-arcuate-premammillary area) on lordosis were observed. These results suggest that brain sites selectively responsive to the facilitatory actions of progesterone exist in the ventromedial-arcuate-premammillary region and that the whole basal hypothalamus participates in the normal, full expression of guinea pig behavioral estrus.     

Morphine pretreatment increases opioid inhibitory effects on maternal behavior

Ongoing maternal behavior in rats is under the inhibitory influence of opiates. Exposure to drugs of abuse may result in a progressive and enduring enhancement of their reinforcing effects. Little attention has been paid to the possibility that puerperal treatment with morphine may lead to sensitization to this drug, ultimately influencing the effects of opiates on maternal behavior. The aim of the present study was to investigate if the abrupt withdrawal of repeated treatment with morphine chlorhydrate (MC) during late pregnancy and early lactation may influence maternal behavior in lactating rats. The premise that a possible change in sensitivity to the inhibitory effect of MC on maternal behavior would last at least until day 17 of lactation without any reinforcement was tested. In addition, the hypothesis that the MC-induced inhibition would be reversed by the opioid antagonist naloxone was also tested. In all experiments female Wistar rats were treated with MC (5.0 mg/kg/day, subcutaneous [s.c.]) or saline for 7 days starting on the 17th day of pregnancy. After the abrupt discontinuation of long-term treatment, animals were acutely challenged with MC (5.0 mg/kg, s.c.) or saline and tested for maternal behavior in three different experimental situations: first, on days 5, 10, and 17 postpartum (Experiment 1); second, on day 17 postpartum (Experiment 2); third, on day 6 postpartum following naloxone pretreatment (1.0 mg/kg; Experiment 3). In Experiment 1, animals were treated for 7 days with morphine and acutely challenged with MC (group MM). Experimental MM animals showed significantly longer latencies for all maternal behavior parameters than all other groups during all observation days. The other groups (treated with MC for 7 days and acutely challenged with saline, group MS; treated with saline for 7 days and acutely challenged with MC, group SM; and treated with saline for 7 days and acutely challenged with saline, group SS) did not differ significantly from one another. In Experiment 2, in which rats were submitted to a single test on day 17 of lactation, the MM group showed significantly longer latencies for all behavioral parameters as compared to group SM. Previous acute naloxone treatment (Experiment 3) reversed the inhibitory effects of MC on maternal behavior in lactating rats. These data suggest that repeated administration of MC to female rats during late pregnancy sensitizes the animals to the inhibitory effects of opioids on rat ongoing maternal behavior.     

Cycloheximide activation of the lordotic response in low-dose, estrogen-treated ovariectomized rats: evidence for modulating inhibitory influences of the limbic system on sexual behavior

This study tested the effect of intracranially injected cycloheximide (CHX), an inhibitor of protein synthesis, on facilitation of sexual receptivity in ovariectomized rats. The rats received 0.5 μg estradiol benzoate (EB), s.c., once daily on days 8 through 12 after ovariectomy (OVX). Either CHX (in 0.5 μl saline) or 0.5 μl saline was injected into the lateral septum (LS), cortical nucleus (ACO) or medial nucleus of the amygdala or medial preoptic area on day 11 after OVX. The dose of EB was insufficient to facilitate lordotic behavior on day 10 or day 12 after OVX unless CHX was injected into the LS or ACO. Injection of saline did not influence lordosis.     

Stimulation of the mesencephalic central gray increases blood prolactin in ovariectomized rats

Systemic or intraventricular administration of opiate compounds induces not only analgesia but also the reciprocal responses of increased prolactin and decreased luteinizing hormone (LH) release. Electrical stimulation of the ventral periaqueductal gray (VPAG) or dorsal raphe nucleus (DRN) also inhibits both pain perception and LH release. In the present experiments prolactin release in response to stimulation of the VPAG-DRN was studied in ovariectomized rats. Stimulation was delivered through chronically implanted bipolar electrodes for 2 h. Blood samples collected at 10-min intervals through an indwelling jugular cannula were assayed for prolactin by radioimmunoassay. Increased release of prolactin followed increased intensity of stimulation (0.5, 1.0, 2.0 mA) in animals pretreated (10 min before initial blood sample) with saline. Naltrexone (3.7 mg/kg, i.v.) pretreatment was ineffective in antagonizing the effect of stimulation. Response to stimulation of the posterior VPAG-DRN was significantly greater than that to stimulation of more anterior VPAG-DRN loci at a current of 1.5 mA but not at 2.0 mA. Stimulation with a current of 0.5 mA was ineffective in releasing prolactin when applied to the VPAG-DRN, but when delivered to the periaqueductal gray directly lateral to the cerebral aqueduct, marked aversive and prolactin responses resulted. Taken together these data indicate that the VPAG in the region of the DRN contains a specific system capable of stimulating prolactin release and that opiate receptors are not interposed between the mesencephalic sites of activation of this pathway and the hypothalamic-hypophyseal portal system.     

Lack of effect of hyperprolactinemia on serotonin turnover in ovariectomized and ovariectomized estrogen-treated rats

Hyperprolactinemia suppresses luteinizing hormone (LH) and prolactin (PRL) secretion under a variety of experimental conditions. The secretion of both of these hormones is regulated at the hypothalamic level by several neurotransmitters, including serotonin (5-HT). Therefore, we examined the effect of hyperprolactinemia on 5-HT neuronal activity in key hypothalamic areas that are rich in 5-HT terminals and which are known to regulate the release of LH and PRL. Young cycling virgin rats were ovariectomized (day 0). From days 11-16, animals were injected with ovine prolactin (oPRL, 4 mg/kg, s.c.) or vehicle every 8 h. On day 14, one-half of the oPRL- and vehicle-treated rats were implanted with 20-mm long Silastic capsules containing estradiol (180 micrograms/ml). On day 16, animals were killed at 08.00, 12.00 or 18.00 h or treated with pargyline (75 mg/kg) and killed 10 min later. Trunk blood was collected and serum was radioimmunoassayed for LH and endogenous rat PRL (rPRL). Brains were removed, frozen, sectioned and the medial preoptic, suprachiasmatic, and arcuate nuclei, median eminence and globus pallidus were microdissected. Serotonin was measured using high pressure liquid chromatographic methodology. We were unable to detect any feedback effect of hyperprolactinemia on 5-HT turnover in any brain area of ovariectomized or ovariectomized estradiol-treated rats at any time of day that we examined. Several potential reasons for the absence of an effect of hyperprolactinemia on serotonergic function are discussed.     

Effects of septal lesions and chronic estrogen treatment on dopamine,GABA and lordosis behavior in male rats

GORDON, J. H., D. M. NANCE, C. J. WALLIS AND R. A. GORSKI. Effects of septal lesions and chronic estrogentreatment on dopamine, GABA and lordosis behavior in male rats. BRAIN RES. BULL. 4(1) 85–89, 1979.—Septal lesions (SL) in female rats result in an increased sensitivity to the behavioral effects of acute estradiol benzoate (ACUTE-EB; 2 μg/day × 3) treatment as measured by the lordosis quotient (LQ; number of lordotic responses × 100/number of mounts). Male rats, intact or castrated, do not show this enhanced behavioral response to ACUTE-EB unless they are treated with EB (2 μg/day) for 2–4 weeks immediately following the production of SL. The present study was undertaken to examine possible neurochemical alterations which could account for the enhanced behavioral sensitivity to ACUTE-EB seen in the SL male rat treated chronically with EB during the postlesion period (SL-EB). Three groups, normal males, SL-EB and SL males chronically treated with oil (SL-oil), were subdivided and treated with ACUTE-EB or oil and decapitated. The brains were removed, frozen and stored at ?50°C prior to dissection and assay. Tyrosine hydroxylase (TH) activity was assayed in the dopamine (DA) rich areas of the forebrain (striatum, STR; nucleus accumbens septi, ACB; and olfactory tubercle). The TH activity was significantly suppressed in both the STR and ACB of the SL-EB males treated with ACUTE-EB. The glutamic acid decarboxylase (GAD) activity in both the substantia nigra and ventral tegmentum was significantly increased in the SL-EB males given ACUTE-EB relative to that of all other groups. In summary, SL-EB males given ACUTE-EB show (1) an enhanced LQ, (2) decreased TH activity in the region of DA terminals, and (3) increased GAD activity in the region of DA cell bodies. The increase in GAD activity is suggested to be a result of an altered neuronal feedback because of plastic changes that occur during chronic EB treatment following production of SL. This probable increase in inhibitory tone in the region of the DA cell bodies may explain the observation that the SL-EB male exhibits decreased DA turnover following ACUTE-EB treatment. Moreover, since DA may be inhibitory to the display of lordosis behavior, the SL-EB males may show an enhanced LQ, at least partially, because of this reduction in DA activity.     

Alterations by estrogen and hypothyroidism in the effects of septal lesions on lordosis behavior of male rats

Earlier experiments indicated that chronic exposure to estradiol benzoate (EB) following septal lesions can increase the subsequent levels of female sexual behavior in male rats tested several months later following priming doses of EB. However, the present study demonstrates that a single injection of a large dose of EB (50 μg) two days after septal destruction did not modify subsequent responsiveness to EB priming in male rats relative to sham operated controls. Yet male rats given 10 daily injections of 5.0 μg EB/day immediately following a septal lesion were more responsive to EB than oil treated controls when tested later for lordosis behavior. Therefore, the capacity for EB to alter the behavioral effects of septal lesions on lordosis behavior in male rats is related to both chronic administration and a period of susceptibility to some action of EB during the immediate post-lesion period. In two additional experiments, chronic hypothyroidism induced by propylthiouracil or thyroidectomy was also found to modify the effects of septal lesions on female sexual behavior of male rats. These latter results indicate that EB is not unique in its capacity to alter the behavioral effects of septal lesions in male rats, and are consistent with the view that both EB and hypothyroidism may interact with some dynamic process associated with recovery from brain lesions.     

雌激素在慢性束缚应激性抑郁发生中的作用(英文)

目的探讨雌激素和kalirin-7在慢性束缚应激性抑郁发生中的作用。方法采用慢性束缚应激性抑郁动物模型,运用强迫游泳测试和免疫组织化学方法,分别检测动物行为学表现及海马中kalirin-7蛋白的表达。结果慢性束缚应激能显著降低动物体重、延长游泳不动时间、抑制海马中kalirin-7蛋白的表达。注射雌激素能明显改善动物抑郁样行为,并且海马kalirin-7表达显著增加。结论慢性束缚应激能诱发产生抑郁样行为,而雌激素替代疗法则能预防慢性束缚应激性抑郁的发生。此外,kalirin-7在防止慢性束缚应激性抑郁的发生中起到重要作用。     

Effects of estrogen on dopamine turnover, glutamic acid decarboxylase activity and lordosis behavior in septal lesioned female rats

Estradiol benzoate (EB) treatment (2.0 μg/day × 3) of septal lesioned adult female rats produces a marked increase in lordosis behavior over similarly treated sham operated animals. In these animals endogenous dopamine (DA) and norepinephrine (NE) levels were measured and turnover rates were estimated following tyrosine hydroxylase inhibition with α-methyltyrosine, in both EB and oil (0.05 ml × 3 days) treated groups. No consistent pattern of change in the level or rate of turnover of NE was noted for any of the treatment groups. No differences in either the level or turnover of DA were seen in the oil treated septal lesioned group, relative both to EB and oil treated sham operated groups. However, in the amygdala, corpus striatum and nucleus accumbens septi of the septal lesioned animals primed with EB there was both a reduction in endogenous levels (20–50%) and a decrease in synthesis rates (30–70%) of DA relative to both EB and oil treated sham operated groups and the oil treated septal lesioned group. The EB treated septal lesioned animals showed a significant negative correlation between DA levels in the corpus striatum and the level of lordosis behavior (r = −.850), supporting the concept of a possible inhibitory role for DA on female sexual receptivity. Glutamic acid decarboxylase (GAD; the rate limiting enzyme in the synthesis of γ-aminobutyric acid (GABA)) activity was measured in the substantia nigra and ventral tegmental region from the same animals. GAD activity was reduced in both areas in the EB primed sham operated animals, while the EB and oil treated septal lesioned groups remained comparable to the oil treated sham operated animals. Because of the proposed existence of a GABA mediated inhibitory neuronal feedback on DA cell bodies in the midbrain, the reduction in DA turnover in the EB primed septal lesioned female rat and thus the increase in behavioral receptivity could be due in part to the failure of the septal lesioned animal to show a compensatory decrease in GAD activity.     

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 3mg coumestrol (CM1, CM3), 1mg genistein (GS1), 1mg estradiol (E2), 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 E2-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 E2-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 E2-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 E2-treated rats. Behavioral tests were carried out after implantation of E2-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, E2 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 1mg coumestrol was effective in only the estrous cycle of female rats.     

双醋瑞因对去卵巢大鼠骨量丢失的干预作用

背景：双醋瑞因是一种新型的白细胞介素1阻滞剂,对绝经后骨质疏松形成过程中的白细胞介素相关因子增强骨吸收的抑制作用目前的报道较少。 目的：验证双醋瑞因对去卵巢大鼠骨量丢失的干预作用。 设计、时间及地点：完全随机分组设计,随机对照实验,于2008-08/11在重庆医科大学实验动物中心实验室完成。 材料：清洁级3月龄雌性SD大鼠40只,随机分为4组：假手术组、去卵巢组、双醋瑞因10,100 mg/(kg•d)组,每组10只。双醋瑞因胶囊(每粒50 mg含双醋瑞因48.1 mg),为昆明积大制药有限公司生产,批号：20070532。 方法：除假手术组外其他3组大鼠分离出双侧卵巢结扎输卵管血管后切除卵巢,假手术组只切除卵巢周围少量脂肪组织,逐层缝合皮肤。去卵巢术后第2天双醋瑞因10,100 mg/(kg•d)组开始灌胃给药,假手术组和去卵巢组给予等量的生理盐水,持续给药10周后麻醉下处死所有大鼠采血,收集骨骼标本。 主要观测指标：以骨密度双能X射线测量仪测量第3腰椎、股骨骨密度;放射免疫法测定骨组织中白细胞介素1β、白细胞介素6水平及血清骨钙素水平。 结果：40只大鼠均进入结果分析。去卵巢组骨密度低于假手术组(P < 0.05),双醋瑞因2个剂量组骨密度高于去卵巢组(P < 0.05)。去卵巢组骨组织中白细胞介素1β、白细胞介素6水平高于假手术组(P < 0.05);双醋瑞因2个剂量组骨组织中白细胞介素1β、白细胞介素6水平低于去卵巢组(P < 0.05)。去卵巢组血清骨钙素水平高于假手术组(P < 0.05);双醋瑞因2个剂量组血清骨钙素水平与去卵巢组相比,差异无显著性意义(P > 0.05)。 结论：雌性大鼠卵巢切除10周后骨量丢失明显,双醋瑞因对去卵巢后大鼠由于骨吸收增强所引起的骨量丢失有干预作用。对成骨细胞介导的骨形成无明显的影响。     

雌激素对去卵巢大鼠中脑黑质多巴胺能神经元的保护作用

目的观察雌激素对去卵巢大鼠中脑黑质多巴胺能神经元的作用,探讨雌激素防治帕金森病的可能性。方法成年雌性大鼠行卵巢切除术、随机分为雌激素组(Ⅰ组)和对照组(Ⅱ组),应用立体定向技术注射六羟基多巴胺(6OHDA)于大鼠中脑黑质,采用免疫组织化学的方法对黑质多巴胺能神经元酪氨酸羟化酶(TH)进行标记并记数阳性细胞。同时,对大鼠进行行为学观测。结果在没有给予雌激素的去卵巢大鼠组,阿朴吗啡(APO)诱导的旋转次数与对照组相比有显著增加(P<0.05)、大鼠中脑黑质TH阳性神经元数目与对照组比较也有显著减少(P<0.01)。结论雌激素对雌性大鼠中脑黑质多巴胺能神经元具有保护作用。     

Neurohormonal mechanisms of the antidepressant effect of ketanserin in ovariectomized rats

In the present study we investigated the effects of chronic administration of m-CPP (0.5 mg/kg, i.p.), a 5-HT_2B/2C receptor agonist, and ketanserin (0.1 mg/kg, i.p.), a 5-HT_2A/2C receptor antagonist, alone or in a combination with 17β-estradiol (0.5 μg per animal, i.m.) over 14 days on depressive behavior and the concentration of different monoamines in the hippocampus in adult ovariectomized (OVX) female rats. Depression-like behavior was assessed using the Porsolt’s test. The concentrations of monoamines and their metabolites were determined using HPLC. We found that chronic ketanserin administration has an antide-pressant effect in OVX rats. Chronic ketanserin administration in combination with 17β-estradiol in OVX females potentiated antidepressant action. The antidepressant effect of ketanserin in OVX rats correlated with the restoration of noradrenergic, serotonergic, and dopaminergic neurotransmission in the hippocampus. Our data indicate a close interaction between the ovary hormonal and serotonergic systems of the brain in mechanisms of depression.     

Importance of central catecholamines in the mediation of lordosis behaviour in ovariectomized rats treated with estrogen and inhibitors of monoamine synthesis

Summary The effect of-methyl-p-tyrosine methylester hydrochloride (-MT) (100 mg/kg i.p.) orp-chlorophenylalanine methylester hydrochloride (PCPA) (150 mg/kg i.p.) on lordosis behaviour in estrogen pretreated spayed rats was investigated. The effect of-MT was studied 1, 2, 4, 8 and 26 hours after the drug injection and the observations after PCPA were done 2, 4, 8, 26 and 50 hours after the injection. Facilitation of lordosis was seen 2–8 hours after both treatments. Biochemical experiments were done in parallel and the injection of either-MT or PCPA resulted in a transient decrease in brain catecholamines which was correlated in time with the facilitation of the lordosis response. Furthermore PCPA resulted in a gradual decline in brain 5-HT. However, when 5-HT depletion was most pronounced and the brain catecholamines had returned to control levels no increase in lordosis behaviour occurred. Our findings suggest a role for central catecholamines in the mediation of lordosis behaviour in ovariectomized estrogen-drug-treated rats.     

Effects of septal lesions and testosterone on lordosis behavior and luteinizing hormone release in female rats

The increased behavioral sensitivity to estrogen following a septal lesion in female rats has previously been found to be blocked by chronic treatment with testosterone propionate (TP) following the lesion. The effects of this chronic treatment on the ability of progesterone (P) to facilitate the secretion of luteinizing hormone (LH) in the spayed septal lesioned rat primed with estradiol benzoate (EB) was tested in the present study. EB was injected and followed 72 hr later with an injection of P. Blood samples for measurement of plasma LH were taken at 1700 hr, 29 and 53 hr after EB and 5 hr after P injection. Although there was no effect of the lesion, TP treatment significantly inhibited LH values after P administration. In a second experiment, spayed septal lesioned or sham operated rats were given either 0.0, 0.5 or 2.0 μg EB followed by 0.5 mg P just 24 hr later. The display of lordosis behavior, tested 4–6 hr after P injection, was significantly greater in septal lesioned than in sham operated rats following priming injections of 0.5 or 2.0 μ EB. This indicates that septal destruction significantly shortened the duration required for estrogen to prepare neural mechanisms for the effect of progesterone on lordosis behavior. Following a similar steroid regime, no differences were found between lesioned and sham operated rats in plasma LH levels in blood samples taken 5 hr after EB or 5 and 29 hr after P injection.