Ovariectomy has minimal effects on neuroadaptations associated with ethanol dependence in female rats

We previously found gender selective alterations in gene expression for GABA_A and NMDA receptors associated with the development of ethanol dependence. Males and females have a differing hormonal environment, including steroid hormone derivatives (neuroactive steroids) that exert effects at GABA_A and NMDA receptors. Therefore, we explored whether the removal of ovarian steroids would alter gender differences in response to chronic ethanol exposure. We found that ovariectomy reduced ethanol drinking levels by 15%, comparable to earlier observations between intact female and male rats. However, investigation of the effects of chronic ethanol exposure on intact versus ovariectomized female rats uncovered few differences in chronic ethanol-induced alterations in selected GABA_A or NMDA receptor subunit peptide levels. In general, findings for both groups of females were similar to previous observations. There was no reduction in GABA_A receptor 1 subunit levels in cerebral cortex in either intact or ovariectomized female rats, in contrast to the significant reduction observed in male rats. In addition, both intact and ovariectomized female rats had increased levels of the NMDA NR1 subunit in cerebral cortex and hypothalamus, but not in hippocampus, whereas ethanol dependent male rats displayed significant increases in the NR1 subunit only in hippocampus. Radioligand binding analysis with [³⁵S]TBPS found no differences in modulation of the GABA_A receptor by neuroactive steroids between ethanol dependent male, intact female or ovariectomized female rats. Seizure susceptibility was not different between intact or ovariectomized female rats during ethanol withdrawal. We did observe differential effects on brain allopregnanolone and plasma corticosterone levels between ethanol dependent intact and ovariectomized female rats, suggesting that ovarian steroids influence HPA axis adaptations to prolonged ethanol exposure. Overall, these data suggest that ovarian steroids do not significantly impact the gender selective alterations of GABA_A and NMDA receptors associated with ethanol dependence.     

Preference for an estrous female over a non-estrous female evinced by female rats requires dihydrotestosterone plus estradiol

The effects were studied of long-term treatment with testosterone metabolites (dihydrotestosterone, DHT, and estradiol, E2, in sc Silastic implants) on preference behavior of ovariectomized female rats for an estrous female over a non-estrous female. For measuring this behavior a residential plus-maze was used which harbored two ovariectomized “stimulus” females on the top of peripheral boxes, one of which was made estrus by injection of estradiol benzoate and progesterone. When both steroids (DHT plus E2) were circulating simultaneously they evoked preference for an estrous female, while neither steroid by itself sufficed. In earlier work with adult male rats castrated on the day of birth, E2 was effective in the absence of DHT. This sex difference, therefore, seems to have arisen before birth. Further, administration of DHT alone caused a profound lack of interest in both “stimulus” females, which cannot be fully explained by the reduced locomotor activity which has been found to be induced by DHT in earlier Studies.     

Potential contribution of prenatal estrogens to the sexual differentiation of mate preferences in mice

The neural mechanisms controlling sexual behavior are sexually differentiated by perinatal actions of gonadal hormones. We recently observed using female mice deficient in alpha-fetoprotein (AFP-KO) and which lack the protective actions of AFP against maternal estrogens, that exposure to prenatal estrogens completely defeminized their potential to show lordosis behavior in adulthood. Therefore, we determined here whether mate preferences were also affected in female AFP-KO mice. We observed a robust preference for an estrous female over an intact male in female AFP-KO mice, which were ovariectomized in adulthood and subsequently treated with estradiol and progesterone, whereas similarly treated WT females preferred the intact male over the estrous female. Gonadally intact WT males preferred the estrous female over the male, but only when visual cues were blocked by placing stimulus animals behind opaque partitions. Furthermore, when given the choice between an intact male and a castrated male, WT females preferred the intact male, whereas AFP-KO females showed no preference. Finally when given the choice between an estrous female and an ovariectomized female, WT males preferred the estrous female whereas AFP-KO females preferred the ovariectomized female or showed no preference depending on whether they could see the stimulus animals or not. Taken together, when AFP-KO females are tested under estrous conditions, they do not show any male-directed preferences, indicating a reduced sexual motivation to seek out the male in these females. However, they do not completely resemble males in their mate preferences suggesting that the male-typical pattern of mate preferences is not solely organized by prenatal estrogens.     

Gender differences in steroid modulation of angiotensin II-induced protein kinase C activity in anterior pituitary of the rat

To investigate whether the various steroid hormones can modulate the basal and angiotensin II-induced protein kinase C (PKC) activity in the anterior pituitary of the rat, female and male intact and ovariectomized female Wistar rats were treated in vivo with estradiol (E2), progesterone (P), dehydroepiandrostendione sulfate (DHEA-S), and pregnenolone sulfate (PREG-S). Estradiol caused the increase of basal PKC activity in intact and ovariectomized females, but did not change the enzyme activity in males. In ovariectomized animals the increase of PKC activity was lower than in intact females. Progesterone decreased PKC activity only in intact animals. DHEA-S strongly enhanced activity of PKC in ovariectomized females. Pregnenolone sulfate did not significantly change PKC function of all studied groups. Incubation with AngII enhanced the PKC activity in intact (without steroid treatment) animals of both genders. In females, AngII and estradiol together rise the PKC-stimulated phosphorylation in greater degree than used separately. Treatment with other investigated steroids reduced the effect of AngII. In intact males every examined hormone turned back the stimulatory effect of AngII on PKC activity. These data suggest that gender differences in PKC activity are likely related to hormonal milieu of experimental animals and may depend in part on the basic plasma level of estrogens.     

Natural or hormone-induced sexual and social behaviors in the female brown lemming (Lemmus trimucronatus)

The behaviors of intact or ovariectomized, estradiol benzoate-treated or estradiol benzoate followed by progesterone-treated female brown lemmings were compared. Intact, diestrous females engaged in more social interactions with a male than did ovariectomized females (Experiment 1). In the first 5 min of a 1-hr mating exposure (Experiment 2, Test A) intact females in natural estrus engaged in more social and sexual behaviors than did ovariectomized females in estrogen-induced estrus. However, during the last 5 min of the 1-hr exposure (Test B) ovariectomized females receiving estrogen alone continued to show high levels of sexual activity with a male partner, while intact estrous females or females receiving estrogen followed by progesterone showed an apparent drop in sexual receptivity and an increase in aggressivity. Aggressive behaviors, as indexed by threat-leap behaviors on the part of the female may increase in the presence of progesterone. Declines in sexual activity, occurring within 1 hr of progesterone injection, were apparently dependent on the interaction of progesterone and copulatory events which may affect both the male and female.     

Prenatal testosterone exposure leads to hypertension that is gonadal hormone-dependent in adult rat male and female offspring

Prenatal testosterone exposure impacts postnatal reproductive and endocrine function, leading to alterations in sex steroid levels. Because gonadal steroids are key regulators of cardiovascular function, it is possible that alteration in sex steroid hormones may contribute to development of hypertension in prenatally testosterone-exposed adults. The objectives of this study were to evaluate whether prenatal testosterone exposure leads to development of hypertension in adult males and females and to assess the influence of gonadal hormones on arterial pressure in these animals. Offspring of pregnant rats treated with testosterone propionate or its vehicle (controls) were examined. Subsets of male and female offspring were gonadectomized at 7 wk of age, and some offspring from age 7 to 24 wk received hormone replacement, while others did not. Testosterone exposure during prenatal life significantly increased arterial pressure in both male and female adult offspring; however, the effect was greater in males. Prenatal androgen-exposed males and females had more circulating testosterone during adult life, with no change in estradiol levels. Gonadectomy prevented hyperandrogenism and also reversed hypertension in these rats. Testosterone replacement in orchiectomized males restored hypertension, while estradiol replacement in ovariectomized females was without effect. Steroidal changes were associated with defective expression of gonadal steroidogenic genes, with Star, Sf1, and Hsd17b1 upregulation in testes. In ovaries, Star and Cyp11a1 genes were upregulated, while Cyp19 was downregulated. This study showed that prenatal testosterone exposure led to development of gonad-dependent hypertension during adult life. Defective steroidogenesis may contribute in part to the observed steroidal changes.     

Ovariectomy attenuates dendritic growth in hormone-sensitive spinal motoneurons

The lumbar spinal cord of rats contains the sexually dimorphic, steroid-sensitive spinal nucleus of the bulbocavernosus (SNB). Dendritic development of SNB motoneurons in male rats is biphasic, initially showing exuberant growth through 4 weeks of age followed by a retraction to mature lengths by 7 weeks of age. The initial growth is steroid dependent, attenuated by castration or aromatase inhibition, and supported by hormone replacement. Dendritic retraction is also steroid sensitive and can be prevented by testosterone treatment, but is unaffected by aromatase inhibition. Together, these results suggest a role for estrogens during the initial growth phase of SNB development. In this study, we tested whether ovarian hormones could support SNB somal and dendritic development. Motoneuron morphology was assessed in normal males and in females perinatally masculinized with dihydrotestosterone and then either ovariectomized or left intact. SNB motoneurons were retrogradely labeled with cholera toxin-HRP at 4 or 7 weeks of age and reconstructed in three dimensions. Initial growth of SNB dendrites was reduced after ovariectomy in masculinized females. However, no differences in dendritic length were seen at 7 weeks of age between intact and ovariectomized masculinized females, and lengths in both groups were significantly lower than those of normal males. Together with previous findings, these results suggest that estrogens are involved in the early growth of SNB dendrites, but not in their subsequent retraction.     

Ovariectomy attenuates dendritic growth in hormone‐sensitive spinal motoneurons

The lumbar spinal cord of rats contains the sexually dimorphic, steroid‐sensitive spinal nucleus of the bulbocavernosus (SNB). Dendritic development of SNB motoneurons in male rats is biphasic, initially showing exuberant growth through 4 weeks of age followed by a retraction to mature lengths by 7 weeks of age. The initial growth is steroid dependent, attenuated by castration or aromatase inhibition, and supported by hormone replacement. Dendritic retraction is also steroid sensitive and can be prevented by testosterone treatment, but is unaffected by aromatase inhibition. Together, these results suggest a role for estrogens during the initial growth phase of SNB development. In this study, we tested whether ovarian hormones could support SNB somal and dendritic development. Motoneuron morphology was assessed in normal males and in females perinatally masculinized with dihydrotestosterone and then either ovariectomized or left intact. SNB motoneurons were retrogradely labeled with cholera toxin‐HRP at 4 or 7 weeks of age and reconstructed in three dimensions. Initial growth of SNB dendrites was reduced after ovariectomy in masculinized females. However, no differences in dendritic length were seen at 7 weeks of age between intact and ovariectomized masculinized females, and lengths in both groups were significantly lower than those of normal males. Together with previous findings, these results suggest that estrogens are involved in the early growth of SNB dendrites, but not in their subsequent retraction. © 2001 John Wiley & Sons, Inc. J Neurobiol 48: 301–314, 2001     

Sexual experience interacts with steroid exposure to shape the partner preferences of rats

A three-phase experiment manipulated sexual experience and hormone exposure (perinatally and in adulthood) in female rats housed individually from weaning so as to limit peripubertal social and sexual experience. Noncontact partner preference for a male or estrous female rat was measured both before and after sexual experience, first while rats were under the influence of circulating testosterone propionate (TP) and later after priming them with ovarian hormones (estradiol benzoate and progesterone; EB & P). When implanted with TP capsules and tested while sexually naive, all groups of female rats preferred females to males without differing statistically. However, following three sexual experience sessions with estrous females, differences emerged between the masculinized and control groups in the magnitude of their female-directed preference, with masculinized females demonstrating a significantly greater preference for estrous females. Sexual experience with male rats under EB & P did not result in a significant shift in preference in any group. Histological assessment indicated that the volume of the sexually dimorphic nucleus of the preoptic area (SDN-POA) was increased by exposure to TP postnatally, and SDN-POA volume correlated positively with partner preference scores but only when rats were both sexually experienced and exposed to circulating TP in adulthood. These results suggest that sexual experience interacts with steroid exposure to shape partner preference.     

Shifts in preferred learning strategy across the estrous cycle in female rats

The current status of the effects of ovarian steroids on learning and memory remains somewhat unclear, despite a large undertaking to evaluate these effects. What is emerging from this literature is that estrogen, and perhaps progesterone, influences learning and memory, but does so in a task-dependent manner. Previously, we have shown that ovariectomized rats given acute treatments of estrogen acquire allocentric or "place" tasks more easily than do rats deprived of estrogen, but acquire egocentric or "response" learning tasks more slowly than do those deprived of hormone, suggesting that estrogen treatment may bias the strategy a rat is able to use to solve tasks. To determine if natural fluctuations in ovarian hormones influence cognitive strategy, we tested whether strategy use fluctuated across the estrous cycle in reproductively intact female rats. We found that in two tasks in which rats freely choose the strategy used to solve the task, rats were more likely to use place strategies at proestrous, that is, when ovarian steroids are high. Conversely, estrous rats were biased toward response strategies. The data suggest that natural fluctuations in ovarian steroids may bias the neural system used and thus the cognitive strategies chosen during learning and memory.     

Gonadal steroids modulated hypocretin/orexin type-1 receptor expression in a brain region, sex and daytime specific manner

Orexins A and B (hypocretins A and B) are regulatory peptides that control a variety of neuroendocrine and autonomic functions including feeding and sleep-wakefulness. Previously, we described a clear relationship between the hormonal milieu of the estrous cycle and the mRNA expression of the components of the orexinergic system, in the hypothalamus, pituitary and ovary. Here, we investigate whether steroid hormones are involved in the modulation of the hypocretin/orexin type-1 receptor expression at the protein level, and its time of the day dependence, in hypothalamus and pituitary of castrated male and female rats and castrated receiving hormone replacement.Orchidectomy decreased the hypocretin/orexin type-1 receptor expression in anterior hypothalamus, but not in mediobasal hypothalamus or cortex; in pituitary this treatment resulted in an increase. Testosterone and dihydrotestosterone were able to restore receptor expression and gonadotropins.In females, pituitary and ovarian hormones increased during proestrous afternoon. Hypocretin/orexin type-1 receptor expression was higher at 19:00 of proestrus in hypothalamus and pituitary. Ovariectomized treated with estradiol or oil and sacrificed at 11:00 h showed the receptor expression similar to 11:00 h of proestrus in hypothalamus and pituitary. At 19:00 h, low expression persisted in these areas in oil-treated ovariectomized rats; in contrast, estradiol replacement increased the expression to high levels of normal cycling rats at 19:00 h.Sexual steroids modulate the orexinergic system and the anatomical regions, hormones and times of the day all have to be considered when the roles of orexins, and probably other peptides, are under consideration.     

Sexual Dimorphism in Development of Kidney Damage in Aging Fischer-344 Rats

BackgroundAging kidneys exhibit slowly developing injury and women are usually protected compared with men, in association with maintained renal nitric oxide.ObjectivesOur purpose was to test 2 hypotheses: (1) that aging intact Fischer-344 (F344) female rats exhibit less glomerular damage than similarly aged males, and (2) that loss of female ovarian hormones would lead to greater structural injury and dysregulation of the nitric oxide synthase (NOS) system in aging F344 rat kidneys.MethodsWe compared renal injury in F344 rats in intact, ovariectomized, and ovariectomized with estrogen replaced young (6 month) and old (24 month) female rats with young and old intact male rats and measured renal protein abundance of NOS isoforms and oxidative stress.ResultsThere was no difference in age-dependent glomerular damage between young or old intact male and female F344 rats, and neither ovariectomy nor estrogen replacement affected renal injury; however, tubulointerstitial injury was greater in old males than in old females. These data suggest that ovarian hormones do not influence these aspects of kidney aging in F344 rats and that the greater tubulointerstitial injury is caused by male sex. Old males had greater kidney cortex NOS3 abundance than females, and NOS1 abundance (alpha and beta isoforms) was increased in old males compared with both young males and old females. NOS abundance was preserved with age in intact females, ovariectomy did not reduce NOS1 or NOS3 protein abundance, and estrogen replacement did not uniformly elevate NOS proteins, suggesting that estrogens are not primary regulators of renal NOS abundance in this strain. Nicotinamide adenine dinucleotide phosphate oxidase-dependent superoxide production and nitrotyrosine immunoreactivity were increased in aging male rat kidneys compared with females, which could compromise renal nitric oxide production and/or bioavailability.ConclusionsThe kidney damage expressed in aging F344 rats is fairly mild and is not related to loss of renal cortex NOS3 or NOS1 alpha.     

Estrogen effects on thyroid iodide uptake and thyroperoxidase activity in normal and ovariectomized rats

Sex steroids interfere with the pituitary-thyroid axis function, although the reports have been controversial and no conclusive data is available. Some previous reports indicate that estradiol might also regulate thyroid function through a direct action on the thyrocytes. In this report, we examined the effects of low and high doses of estradiol administered to control and ovariectomized adult female rats and to pre-pubertal females. We demonstrate that estradiol administration to both intact adult and pre-pubertal females causes a significant increase in the relative thyroid weight. Serum T3 is significantly decreased in ovariectomized rats, and is normalized by estrogen replacement. Neither doses of estrogen produced a significant change in serum TSH and total T4 in ovariectomized, adult intact and pre-pubertal rats. The highest, supraphysiological, estradiol dose produced a significant increase in thyroid iodide uptake in ovariectomized and in pre-pubertal rats, but not in control adult females. Thyroperoxidase activity was significantly higher in intact adult rats treated with both estradiol doses and in ovariectomized rats treated with the highest estradiol dose. Since serum TSH levels were not significantly changed, we suggest a direct action of estradiol on the thyroid gland, which depends on the age and on the previous gonad status of the animal.     

Taste aversions in the ontogeny of the rat

The characteristics of acquisition and extinction of conditioned taste aversion (CTA) were studied in rats of both sexes and various ages by pairing of saccharin solution consumption with discomfort (LiCl intoxication, rotation). Pairing of saccharin consumption with LiCl in adult rats led to acquisition of CTA, more profound in male rats than in female ones. In rats of both sexes 30 days old, a profound CTA, comparable in intensity with CTA of adult male rats was acquired. In 2 months after acquisition of CTA in adult rats its magnitude did not change, while in rats of the junior group which by that time had reached puberty, CTA was reduced in females and did not change in males. Pairing of saccharin intake and rotation led to acquisition of CTA only in rats 30 days old. The role of external factors in duration of retention of CTA acquired by pairing of saccharin solution consumption with LiCl injection was studied in male and female rats 1 and 3.5 months old. In all cases CTA was extinguished much sooner in home cages than in experimental chambers, and in the elder group sex dimorphism was found: in both situations CTA disappeared sooner in female rats. The obtained data allow to suggest modulating influences of hormonal background and of contextual stimuli on CTA acquisition and retention.     

Effects of D2 receptor agonist and antagonist on behavior of intact and ovariectomized rats

The involvement of D2 dopaminergic receptors in behavioral responses during ovary cycle was assessed in adult intact female rats and ovariectomized (OVX) female rats. Quinperole (0.1 mg/kg), D2 receptor agonist and sulpiride (10.0 mg/kg), D2 receptor antagonist were injected chronically to adult intact and ovariectomized (OVX) female rats either separately or in combination with 17beta-estradiol (0.5 microg) within 14 days. Behavior of these animals was assessed in the "open field" test, whereas passive avoidance performance served as a model of learning. In intact rats, the passive avoidance performance was observed only in metestrous and diestrous. Chronic quinperole administration to intact females resulted in the appearance of the passive avoidance performance in proestrous and estrous, as distinct from the control animals. The passive avoidance performance was not reproduced in OVX rats. Quinperole per se or in combination with 17beta-estradiol completely restored the passive avoidance performance in OVX rats. Moreover, quinperole or sulpiride administration to OVX rats increased horizontal locomotor activity, exploratory behavior, and grooming behavior.     

Adrenal contribution to the induction of sexual behavior in the female musk shrew.

Sexually experienced female musk shrews (Suncus murinus) lack an ovarian, vaginal, and behavioral estrous cycle. Females, once induced by their initial contact with a male, are able to display copulatory behavior whenever a male is present (Rissman, Silveira, and Bronson, 1988). Based on plasma levels of steroids, and on hormone replacement studies conducted after ovariectomy (OVX), we have shown that testosterone (T) plays an essential role in the regulation of female sexual behavior (Rissman and Crews, 1988; Rissman, Clendenon, and Krohmer, 1990a; Rissman, 1991). To date we have only examined the potential contribution of adrenal steroids to female sexual behavior in a preliminary manner. After adrenalectomy, gonadally intact females display significantly lower levels of sexual behavior than controls (Rissman and Bronson, 1987). The following experiments were conducted to examine the role the adrenal steroids (in contrast to the medullary hormones) play in the induction of female sexual behavior in the musk shrew. In the first experiment gonadally intact females were treated with dexamethasone (DEX) to reduce the secretion of adrenal steroids. Significantly fewer females receiving DEX demonstrated sexual behavior as compared with controls. In the second study, OVX females received T-filled Silastic implants. When DEX was administered to OVX + T females at a dose that dropped circulating T levels to those found in ovary and adrenal intact females, no effect on sexual behavior was noted. The data show that the adrenals are a behaviorally important source of T and contribute toward the hormonal control of sexual behavior in these female mammals.     

Dopaminergic metabolism in carotid bodies and high-altitude acclimatization in female rats

We tested the hypothesis that ovarian steroids stimulate breathing through a dopaminergic mechanism in the carotid bodies. In ovariectomized female rats raised at sea level, domperidone, a peripheral D2-receptor antagonist, increased ventilation in normoxia (minute ventilation = +55%) and acute hypoxia (+32%). This effect disappeared after 10 daily injections of ovarian steroids (progesterone + estradiol). At high altitude (3,600 m, Bolivian Institute for High-Altitude Biology-IBBA, La Paz, Bolivia), neutered females had higher carotid body tyrosine hydroxylase activity (the rate-limiting enzyme for catecholamine synthesis: +129%) and dopamine utilization (+150%), lower minute ventilation (-30%) and hypoxic ventilatory response (-57%), and higher hematocrit (+18%) and Hb concentration (+21%) than intact female rats. Consistent signs of arterial pulmonary hypertension (right ventricular hypertrophy) also appeared in ovariectomized females. None of these parameters was affected by gonadectomy in males. Our results show that ovarian steroids stimulate breathing by lowering a peripheral dopaminergic inhibitory drive. This process may partially explain the deacclimatization of postmenopausal women at high altitude.     

Endocrine characterization of a human ovarian carcinoma (BG-1) established in nude mice

The steroid receptor-positive human ovarian cancer (BG-1) was evaluated to determine its usefulness as a tumor model. This tumor grows in intact male and female nude mice without hormone supplements. Moreover, its growth was significantly accelerated in ovariectomized mice, and the increased growth rate could be reversed by estradiol administration. Evaluation of tumor growth following endocrine therapy revealed that, while antiandrogens did not affect the tumor growth, both an aromatase inhibitor and a luteinizing hormone-releasing hormone agonist significantly impaired growth of this human ovarian tumor. Estradiol was also shown to up-regulate both estrogen and progesterone receptors in tumors grown in ovariectomized mice. Therefore, the BG-1 human ovarian carcinoma grows without hormonal supplements and yet responds to specific forms of endocrine therapy. Moreover, the steroid receptors present in this tumor respond to exogenous steroids. In conclusion, this tumor may serve as an ideal model for the study of hormonal regulation of ovarian tumor growth.     

Estrogen and progestagens differentially modulate vascular proinflammatory factors

The potential benefit of ovarian hormone replacement therapy in cerebrovascular disease is well supported by experimental observations but not by recent large, randomized clinical trials. This discrepancy points out the need for better understanding of the vascular actions of ovarian hormones as well as medroxyprogesterone acetate (MPA), a synthetic analog of progesterone (P) widely prescribed in combination with estrogens. Therefore, we investigated whether in vivo exposure to 17beta-estradiol (E) and/or P or MPA modifies inflammation in the cerebral vasculature, a key process in the evolution of ischemic brain injury. Female rats were injected (ip) with LPS to induce inflammation, and 6 h later brains were taken for blood vessel isolation and Western blot analysis of the inflammatory enzymes inducible NO synthase (iNOS) and cyclooxygenase-2 (COX-2). In ovariectomized (O) females, LPS induced cerebrovascular iNOS and COX-2; however, this effect was significantly decreased when O animals were treated for 3 wk with E. In contrast, treatment of O females with either MPA or P exacerbated the cerebrovascular inflammatory response to LPS. In intact females, LPS induction of iNOS and COX-2 in cerebral vessels was found to vary with the stage of the estrous cycle: LPS had the greatest effect during estrus, when circulating estrogen is low and progesterone is high. Thus exposure to endogenous or exogenous ovarian hormones appears to modulate cerebrovascular inflammation. Anti-inflammatory effects of estrogen would attenuate ischemic brain injury; however, this vasoprotective benefit may be diminished in the presence of progestagens.     

Morphological and functional study of the GH-immunoreactive adenohypophyseal cells in ovariectomized rats

Summary In view of the existence of a different secretion pattern of growth hormone (GH) between male and female rats, the aim of the present study was to analyse the role played by ovarian steroid hormones in the modulation of such secretion. To do so, postpuberal female rats were ovariectomized and killed at 30 days after the operation. The basal serum levels of growth hormone, together with cell area, cytoplasmic area and nuclear area of the hypophyseal somatotropic cells of normal and ovariectomized rats were compared. The results obtained show that ovariectomy induces a significant decrease (p<0.05) in the basal serum levels of GH, accompanied by an increase in cellular and cytoplasmic areas, with no significant differences in nuclear area. Overiectomy was also accompanied by an increase in reaction intensity and the number of GH-immunoreactive cells (p<0.01). These findings point to the shift towards a masculine secretory and morphological pattern following ovariectomy and supports the hypothesis that ovarian steroids intervene in the establishment of a different pattern in females compared to males.