Effects of aging on prolactin release after stress in female and male rats

1984 ◽  
Vol 107 (3) ◽  
pp. 337-339 ◽  
Author(s):  
Ljiljana Milenković ◽  
Ljubica Bogić ◽  
Biljana Mušicki ◽  
Jovo V. Martinović
Keyword(s):  
Acute Stress ◽  
Female Rats ◽  
Male Rats ◽  
Elderly Male ◽  
Prolactin Release ◽  
Response To Stress ◽  
Reverse Relationship ◽  
Effects Of Aging ◽  
Sexually Mature ◽  
Intact Rats

Abstract. Young adult and elderly male and female intact rats, as well as chronically ovariectomized (OVX) young and elderly female rats, were subjected to an acute stress by cutting the tip of the tail and prolactin (Prl) concentrations were measured in their blood collected by decapitation at various times thereafter. Maximum concentrations of the hormone were markedly lower in all the three groups of elderly rats than those found in the corresponding young animals, and appeared to occur with a delay in the females, but not in the males. In addition, the Prl-response to stress was attenuated in OVX animals regardless of their age. The result of these experiments, performed at two points on the age scale, suggests that in sexually mature rats of both sexes the stress-induced secretion of Prl is inversely related to the age of the animal and that the reverse relationship is retained in OVX females.

scholarly journals Kisspeptin Stimulation of Prolactin Secretion Requires Kiss1 Receptor but Not in Tuberoinfundibular Dopaminergic Neurons

Endocrinology ◽  
2019 ◽  
Vol 160 (3) ◽  
pp. 522-533 ◽  
Author(s):  
Nayara S S Aquino ◽  
Ilona C Kokay ◽  
Carolina Thörn Perez ◽  
Sharon R Ladyman ◽  
Patricia C Henriques ◽  
...  
Keyword(s):  
Dopaminergic Neurons ◽  
Prolactin Secretion ◽  
Female Rats ◽  
Male Rats ◽  
Prolactin Release ◽  
Whole Cell Patch Clamp ◽  
Neuropeptide Ff ◽  
Concomitant Reduction ◽  
Prolactin Response

Abstract Kisspeptin has been shown to stimulate prolactin secretion. We investigated whether kisspeptin acts through the Kiss1 receptor (Kiss1r) to regulate dopamine and prolactin. Initially, we evaluated prolactin response in a Kiss1r-deficient mouse line, in which Kiss1r had been knocked into GnRH neurons (Kiss1r−/−R). Intracerebroventricular kisspeptin-10 (Kp-10) increased prolactin release in wild-type but not in Kiss1r−/−R female mice. In ovariectomized, estradiol-treated rats, the Kiss1r antagonist kisspeptin-234 abolished the Kp-10–induced increase in prolactin release but failed to prevent the concomitant reduction in the activity of tuberoinfundibular dopaminergic (TIDA) neurons, as determined by the 3,4-dihydroxyphenylacetic acid/dopamine ratio in the median eminence. Using whole-cell patch clamp recordings in juvenile male rats, we found no direct effect of Kp-10 on the electrical activity of TIDA neurons. In addition, dual-label in situ hybridization in the hypothalamus of female rats showed that Kiss1r is expressed in the periventricular nucleus of the hypothalamus (Pe) and arcuate nucleus of the hypothalamus (ARC) but not in tyrosine hydroxylase (Th)–expressing neurons. Kisspeptin also has affinity for the neuropeptide FF receptor 1 (Npffr1), which was expressed in the majority of Pe dopaminergic neurons but only in a low proportion of TIDA neurons in the ARC. Our findings demonstrate that Kiss1r is necessary to the effect of kisspeptin on prolactin secretion, although TIDA neurons lack Kiss1r and are electrically unresponsive to kisspeptin. Thus, kisspeptin is likely to stimulate prolactin secretion via Kiss1r in nondopaminergic neurons, whereas the colocalization of Npffr1 and Th suggests that Pe dopaminergic neurons may play a role in the kisspeptin-induced inhibition of dopamine release.

Permissive role of corticotropin-releasing factor in the acute stress-induced prolactin release in female rats

1995 ◽  
Vol 198 (2) ◽  
pp. 146-148 ◽  
Author(s):  
Tatsuo Akema ◽  
Atsuhiko Chiba ◽  
Morihiro Oshida ◽  
Fukuko Kimura ◽  
Jun-ichi Toyoda
Keyword(s):  
Acute Stress ◽  
Corticotropin Releasing Factor ◽  
Female Rats ◽  
Prolactin Release ◽  
Permissive Role

Effects on growth and body composition of androgen deprivation by castration or autoimmunization to LH-releasing hormone in the male rat under conditions of controlled food intake

1986 ◽  
Vol 110 (1) ◽  
pp. 97-102 ◽  
Author(s):  
J. M. Fletcher ◽  
G. E. Lobley ◽  
A. Connell
Keyword(s):  
Body Composition ◽  
Food Intake ◽  
Gonadal Hormones ◽  
Female Rats ◽  
Male Rats ◽  
Releasing Hormone ◽  
Energy Retention ◽  
Lh Releasing Hormone ◽  
Testicular Steroids ◽  
Intact Rats

ABSTRACT The effects of endogenous gonadal hormones on the regulation of body composition and energy retention have been investigated under conditions of controlled food intake. Male and female rats were fed the same amount from weaning to 82 days of age. The carcases of males contained more protein, less lipid and yielded more ash than females, but they had the same amount of total energy in their carcases as females. In a second experiment, male rats were sham-operated or castrated at 19 days and then fed equal amounts from weaning. At 40 days, intact and castrated rats did not differ in total carcase energy content nor in carcase composition. At 82 days the carcases of intact rats had more protein but had retained the same amount of energy as castrated rats. By 131 days, the difference in protein content was larger and intact rats had less carcase lipid, less carcase energy and gave less ash than castrated rats. At the same age and with a similar food intake, the differences in carcase composition between intact males and females were considerably larger than between intact and castrated males. In a third experiment, male rats were sham-operated or castrated at 1 day post partum and fed the same amount as in the second experiment from weaning to 82 days. Both sham-castrated and castrated rats grew less well than rats operated on at 19 days. The differences in carcase composition between intact and castrated rats were in the same direction but of greater magnitude than in rats operated at the later age. In a fourth experiment the effects on body compositon and energy retention of sham-operation, castration or immunization to LH-releasing hormone (LHRH) at weaning were compared in male rats fed the same amount from weaning to 131 days. Intact rats retained less carcase energy, less lipid and produced less ash than castrated and LHRH-immunized animals. Castrated and LHRH-immunized rats did not differ in carcase composition or amount of energy retained. It is concluded that (1) endogenous sex steroids affect growth and carcase composition independently of food intake, (2) the characteristic carcase composition of the female rat is largely due to the presence of ovarian steroids rather than lack of testicular steroids, (3) in the absence of increased food intake the effects of testicular steroids upon growth and energy expenditure are small but similar to those found in animals with free access to food, (4) the long-terms effects of perinatal exposure to testicular steroids upon growth and carcase composition are not only a consequence of changed food intake and (5) surgical castration and functional castration, induced by LHRH auto-immunization, produce the same effects on carcase composition. J. Endocr. (1986) 110, 97–102

PROLACTIN STIMULATION TEST WITH PERPHENAZINE: AN EVALUATION OF PLASMA PROLACTIN LEVELS AND PITUITARY SECRETORY ACTIVITY IN THE RAT

1976 ◽  
Vol 68 (3) ◽  
pp. 355-368 ◽  
Author(s):  
A. A. VAN DER GUGTEN ◽  
P. C. SAHULEKA ◽  
G. H. VAN GALEN ◽  
H. G. KWA
Keyword(s):  
Adult Male ◽  
Secretory Activity ◽  
Female Rats ◽  
Male Rats ◽  
Plasma Prolactin ◽  
Prolactin Release ◽  
Oestrogen Treatment ◽  
Endocrine Status ◽  
Pituitary Prolactin ◽  
Single Plasma

SUMMARY Many investigations of the regulation of prolactin synthesis and release are based on single plasma prolactin determinations. The purpose of the present experiment was to ascertain whether groups of rats (i.e. young or adult, male or female animals, being either intact, gonadectomized or gonadectomized and treated with oestrone), differing in age and/or endocrine status, will react to a single dose of perphenazine by an acute release of pituitary prolactin in proportion to their initial plasma prolactin levels. No consistent relation existed between the classification of the twelve groups of rats into three categories of basal plasma prolactin levels (i.e. < 20, 25–50, > 125 ng/ml) and their response to perphenazine. Even though all groups showed a highly significant increase of plasma prolactin levels the magnitude of the maximum prolactin response at 30 min varied greatly within the groups of one category and thus was not related to the initial prolactin levels. The effect of 14 days of oestrone treatment in increasing plasma prolactin levels in gonadectomized animals was greatest in young and adult male rats, less in young females and not significant in adult females. The results obtained after perphenazine treatment in the latter group made it clear that the effect of oestrogen treatment on prolactin release can be completely blocked by increasing synthesis and/or release of the prolactin-release inhibiting factor (PIF). Since perphenazine induces decrease of pituitary prolactin and a concomitant increase of plasma prolactin levels through lowered PIF-action, the positive effect of oestrogens on prolactin release (as observed in gonadectomized male and young female rats) apparently is caused by a different mode of action. The implications of these findings for the regulation of prolactin release, as affected by the endocrine status of the rat, is discussed. Moreover, comparison of prolactin lost from the pituitary and gained in the circulation of the experimental animals, with amounts of prolactin that were observed to disappear from plasma during the experiment, provided suggestive evidence that the capacity to synthesize and/or eliminate prolactin, after a sudden provoked release of the hormone, differed among the groups. The rates of synthesis by the pituitary, of release from the pituitary into the circulation as well as of elimination of the hormone from the circulation (equally involved in determining actual plasma levels) are thought, therefore, to be far more important for the elucidation of prolactin regulation than single plasma prolactin determinations.

scholarly journals Rats Lacking Dopamine Transporter Display Increased Vulnerability and Aberrant Autonomic Response to Acute Stress

Biomolecules ◽  
2020 ◽  
Vol 10 (6) ◽  
pp. 842
Author(s):  
Placido Illiano ◽  
Gregory E. Bigford ◽  
Raul R. Gainetdinov ◽  
Marta Pardo
Keyword(s):  
Dopamine Transporter ◽  
Hpa Axis ◽  
Acute Stress ◽  
Female Rats ◽  
Autonomic Response ◽  
Before And After ◽  
Response To Stress ◽  
Vulnerability To Stress ◽  
Body Temperature Increase ◽  
Reduced Temperature

The activity of the hypothalamus–pituitary–adrenal (HPA) axis is pivotal in homeostasis and presides the adaptative response to stress. Dopamine Transporter (DAT) plays a key role in the regulation of the HPA axis. We used young adult female DAT Knockout (KO) rats to assess the effects of DAT ablation (partial, heterozygous DAT+/-, or total, homozygous DAT-/-) on vulnerability to stress. DAT-/- rats show profound dysregulation of pituitary homeostasis, in the presence of elevated peripheral corticosterone, before and after acute restraint stress. During stress, DAT-/- rats show abnormal autonomic response at either respiratory and cardiovascular level, and delayed body temperature increase. DAT+/- rats display minor changes of hypophyseal homeostatic mechanisms. These rats display a similar pituitary activation to that of the control animals, albeit in the presence of higher release of peripheral corticosterone than DAT-/- after stress, and reduced temperature during stress. Our data indicate that DAT regulates the HPA axis at both the central and peripheral level, including autonomic function during stress. In particular, the partial deletion of DAT results in increased vulnerability to stress in female rats, which display central and peripheral alterations that are reminiscent of PTSD, and they might provide new insights in the pathophysiology of this disorder.

A sex difference in endogenous opioid regulation of the posterior pituitary response to stress in the rat

1986 ◽  
Vol 111 (2) ◽  
pp. 239-244 ◽  
Author(s):  
D. A. Carter ◽  
T. D. M. Williams ◽  
S. L. Lightman
Keyword(s):  
Sex Difference ◽  
Gonadal Hormones ◽  
Endogenous Opioids ◽  
Female Rats ◽  
Male Rats ◽  
Posterior Pituitary ◽  
Endogenous Opioid ◽  
Chronic Morphine ◽  
Response To Stress ◽  
Naloxone Treatment

ABSTRACT The influence of endogenous opioids on the posterior pituitary response to stress was investigated by measuring plasma hormone levels in immobilized male and female rats following either acute naloxone treatment or prolonged morphine administration. Naloxone significantly potentiated the oxytocin and arginine vasopressin (AVP) response to immobilization, but in female rats only. The responses of morphine-treated male rats showed differences compared with vehicle-treated controls, although chronic morphine treatment did not reliably alter the oxytocin or AVP responses to immobilization in males or females. In a further experiment to investigate the role of gonadal hormones in determining the sex difference in responsiveness to naloxone, it was found that acute naloxone treatment significantly potentiated the posterior pituitary response to stress in castrated male rats. These results extend previous studies showing a sex difference in stress-induced secretion of posterior pituitary hormones, providing evidence of a sexual dimorphism in the endogenous opioid regulation of this response which is partly determined by circulating gonadal hormones. J. Endocr. (1986) 111, 239–244

A FEMALE-LIKE RISE IN LUTEINIZING HORMONE AND FOLLICLE-STIMULATING HORMONE AFTER GONADECTOMY IN MALE RATS INDUCED BY OESTRADIOL PRETREATMENT

1979 ◽  
Vol 80 (1) ◽  
pp. 111-116 ◽  
Author(s):  
S. N. JUSTO ◽  
A. NEGRO-VILAR
Keyword(s):  
Sexual Difference ◽  
Female Rats ◽  
Male Rats ◽  
Ovariectomized Rats ◽  
Serum Concentrations ◽  
Control Male ◽  
Male And Female Rats ◽  
Series Of Experiments ◽  
And Control ◽  
Intact Rats

A marked sexual difference in the rise of serum gonadotrophin concentrations after gonadectomy has been described in the rat. Gonadectomy in males induced a rapid rise in the concentrations of both LH and FSH within 8 to 12 h, whereas ovariectomy invoked a rapid increase in the concentration of FSH while the response by LH was delayed for several days. To determine whether these differences could be explained, at least in part, by the different steroid milieu at the time of gonadectomy, a series of experiments were performed to analyse the rise in both LH and FSH serum concentrations in control male and female rats and in male rats that had been pretreated with oestradiol-17β. Adult male rats received an s.c. implant of a silicone elastomer capsule filled with crystalline oestradiol-17 β. Controls received empty capsules. Twenty-four hours later, the oestradiol-implanted rats were castrated and control animals were sham-operated. Both LH and FSH levels remained within control levels after castration in the oestradiol-implanted rats, indicating that the oestradiol implant was preventing any rise of either gonadotrophin. On day 5 after implantation, the capsules were removed, sham-implanted animals were castrated and LH and FSH levels at 12, 24, 48 and 72 h were measured and compared with those of ovariectomized rats at similar intervals. The control male rats displayed the pattern of gonadotrophin increments normally found after castration, with both LH and FSH concentrations rising significantly by 12 h after castration and with further increments at later periods. Oestradiol-treated rats showed a female-like gonadotrophin pattern. FSH levels started to rise significantly at 24 h compared with values from intact rats and increased further at 48 and 72 h. During the first 48 h, FSH levels in both oestradiol-treated, castrated rats and female gonadectomized rats were significantly lower than in castrated animals. LH levels, on the other hand, remained low in both groups during the first 48 h, starting to rise significantly above control levels by 72 h. These results indicate that the different pattern of response to gonadectomy in rats of both sexes may be altered by changes in steroid environment and, therefore, may not be genetically predetermined.

Sex and estrous cycle differences in the behavioral effects of high-strength static magnetic fields: role of ovarian steroids

2006 ◽  
Vol 290 (3) ◽  
pp. R659-R667 ◽  
Author(s):  
Angie M. Cason ◽  
Megan DenBleyker ◽  
Kimberly Ferrence ◽  
James C. Smith ◽  
Thomas A. Houpt
Keyword(s):  
Magnetic Fields ◽  
Estrous Cycle ◽  
Hormone Replacement ◽  
High Strength ◽  
Behavioral Effects ◽  
Female Rats ◽  
Male Rats ◽  
Static Magnetic Fields ◽  
Ovarian Steroids ◽  
Intact Rats

Advances in magnetic resonance imaging are driving the development of higher-resolution machines equipped with high-strength static magnetic fields (MFs). The behavioral effects of high-strength MFs are largely uncharacterized, although in male rats, exposure to 7 T or above induces locomotor circling and leads to a conditioned taste avoidance (CTA) if paired with a novel taste. Here, the effects of MFs on male and female rats were compared to determine whether there are sex differences in behavioral responses and whether these can be explained by ovarian steroid status. Rats were given 10-min access to a novel saccharin solution and then restrained within a 14-T magnet for 30 min. Locomotor activity after exposure was scored for circling and rearing. CTA extinction was measured with two-bottle preference tests. In experiment 1, males were compared with females across the estrous cycle after a single MF exposure. Females circled more and acquired a more persistent CTA than males; circling was highest on the day of estrus. In experiment 2, the effects of three MF exposures were compared among intact rats, ovariectomized females, and ovariectomized females with steroid replacement. Compared with intact rats, ovariectomy increased circling; estrogen replacement blocked the increase. Males acquired a stronger initial CTA but extinguished faster than intact or ovariectomized females. Thus the locomotor circling induced by MF exposure was increased in females and modulated by ovarian steroids across the estrous cycle and by hormone replacement. Furthermore, female rats acquired a more persistent CTA than male rats, which was not dependent on estrous phase or endogenous ovarian steroids.

Incidence, growth and oestradiol-receptor levels of 7,12-dimethylbenz(a)anthracene-induced mammary tumours in rats: effects of neonatal sex steroids and oestradiol implants

1982 ◽  
Vol 95 (3) ◽  
pp. 357-368 ◽  
Author(s):  
G. Verhoeven ◽  
G. Vandoren ◽  
W. Heyns ◽  
E. R. Kühn ◽  
J. P. Janssens ◽  
...  
Keyword(s):  
Female Rats ◽  
Male Rats ◽  
Intact Female ◽  
Intact Male ◽  
Tumour Incidence ◽  
Tumour Induction ◽  
Male And Female Rats ◽  
Neonatal Administration ◽  
Low Levels ◽  
Intact Rats

The effects of neonatally administered steroids on the sensitivity of the mammary gland to tumour induction by 7,12-dimethylbenz(a)anthracene was studied as a model for delayed (de)differentiating effects of steroid hormones. Immediately after birth male and female rats were gonadectomized and treated with testosterone, oestradiol or oil. Control animals were left intact. On day 45 all the gonadectomized animals and some of the control animals received an implant which delivered continuous low levels of oestradiol. The carcinogen was administered on day 55. The administration of an oestradiol implant, which increased prolactin levels in all animals, markedly reduced tumour incidence in intact female rats and increased tumour incidence in intact male rats. Neonatal administration of testosterone or oestradiol did not significantly influence tumour incidence, histopathology or oestradiol responsiveness in neonatally gonadectomized rats but tended to decrease tumour oestradiol-receptor levels. This lack of effect of neonatal steroids in gonadectomized animals suggests that the effects observed by other authors in intact rats are mediated by changes in gonadal secretions. It is concluded that the hormonal environment during and after tumour induction plays a major role in the development of 7,12-dimethylbenz(a)anthracene-induced mammary carcinomas.

CORRELATION BETWEEN THE EFFECTS OF NEUROLEPTICS ON PROLACTIN RELEASE, MAMMARY STIMULATION AND THE VAGINAL CYCLE IN RATS

1978 ◽  
Vol 76 (3) ◽  
pp. 507-515 ◽  
Author(s):  
W. LOTZ ◽  
R. KRAUSE
Keyword(s):  
Mammary Gland ◽  
Dose Dependence ◽  
Clinical Syndrome ◽  
Female Rats ◽  
Male Rats ◽  
Test Model ◽  
Neuroleptic Drugs ◽  
Prolactin Release ◽  
Luteinizing Hormone Releasing Hormone ◽  
Daily Oral Administration

The correlation between hyperprolactinaemia induced by the administration of neuroleptic drugs, disturbances of the vaginal cycle and mammary gland stimulation in rats was investigated as a test model simulating the clinical syndrome of hyperprolactinaemia and amenorrhoea with anovulation. In acute experiments in which clozapine, sulpiride and chlorpromazine were administered orally to rats of both sexes, there were rapid increases in the level of prolactin in the serum with peak values between 15 and 60 min. The responses of female rats to various doses of sulpiride were consistently higher than those of male rats. Hyperprolactinaemia induced by sulpiride in dioestrous rats failed to desensitize the ovaries to the ovulatory effect of exogenous luteinizing hormone releasing hormone. Studies of these substances and of metoclopramide, haloperidol and thioridazine were then carried out in female rats by daily oral administration over a period of 13 days. The increases in the level of prolactin in the serum were paralleled by disruption of the vaginal cycle up to and including constant dioestrus and by mammary gland stimulation which, like the preceding phenomena, showed dose-dependence. The potencies of these six neuroleptics, as estimated from their effects on the mammary gland, appeared to be haloperidol&#x2AA2; sulpiride ≥ metoclopramide = thioridazine > chlorpromazine > clozapine.

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