摘要:

The role of the vomeronasal organ (VNO) in the male-induced enhancement of sexual receptivity in ovariectomized estrogen-primed rats was investigated. Removal of the VNO significantly reduced the enhancement of sexual receptivity following mating, as compared with the sham-operated controls. The sham-operated females exhibited a surge of luteinizing hormone (LH) following mating; however, LH release induced by pairing with males was less manifested in the VNO-removed females. This suggests that in female rats, VNO removal impairs the male-induced release of LH-releasing hormone (LHRH). Since LHRH enhances sexual receptivity in ovariectomized estrogen-primed rats, the present results suggest that the increase in sexual receptivity in female rats following mating probably results from a VNO-mediated LHRH release.

ISSN:0028-3835    

DOI:10.1159/000125619

出版商:S. Karger AG    

年代:1990

数据来源: Karger

摘要:

Previous work established that intravenous administration of the opioid receptor antagonist naloxone abruptly increased release of luteinizing hormone (LH) and decreased release of prolactin (PRL) in suckled anestrous ewes and also increased LH release in cyclic luteal ewes. The goal of the present research was to identify brain sites at which local unilateral infusions of naloxone would consistently duplicate the previously noted effects of intravenous naloxone. Intracerebral guide tubes were surgically implanted into the brain of 13 nonpregnant and 16 pregnant ewes at least 4 weeks prior to experimentation. Intracerebral infusion (20–40 µl each through an inner cannula) was performed once daily during postpartum anestrus in suckled fall-lambing ewes and during recurring luteal states of the estrous cycle. Naloxone infusion (n = 142) usually consisted of 50 or 100 µg naloxone, although 5 ewes received 200 and 400 µg per infusion. Control infusions (n = 103) consisted of the vehicle for naloxone (i.e., 0.9% NaCl). Serum concentrations of LH and PRL were quantified at 10-min intervals from 90 min before to 100 min after infusion. Hormone data from individual ewes were grouped for least-squares analysis of variance based upon postmortem neuroanatomical identification of each infusion site. Unilateral intracerebral administration of naloxone consistently induced an increase in LH release within 20 min in the following two neuroanatomical groups: basal forebrain (n = 9 ewes) and chiasmatic area (n = 4 ewes). These naloxone-sensitive brain areas constituted an apparent continuum of tissue sites located as far rostral as ventrolateral septum, diagonal band of Broca and nucleus accumbens and continuing caudally into the preoptic area in and around the organum vasculosum of the lamina terminalis. Brain sites at which the present unilateral infusions of naloxone did not consistently stimulate release of LH included those hypothalamic areas caudal to the preoptic area such as anterior, ventromedial and lateral hypothalamic area including the arcuate nucleus and third ventricle. Therefore, neuroanatomical sites at which local unilateral infusion of naloxone stimulated (i.e., disinhibited) release of LH were very similar to the location of LH-releasing hormone (LHRH) perikarya reported by others for the ovine brain and quite distant from the pituitary gland. Although intravenous naloxone was shown previously to decrease PRL release in suckled anestrous ewes, the present infusion of naloxone did not consistently affect PRL release in such ewes. In summary, local unilateral antagonism of opioid receptors in the vicinity of LHRH perikarya was sufficient to disinhibit release of LHRH/LH, but opioid mechanisms stimulatory to PRL release were not antagonized by intracerebral infusions of nalo

ISSN:0028-3835    

DOI:10.1159/000125620

出版商:S. Karger AG    

年代:1990

数据来源: Karger

摘要:

Experiments were conducted to determine if endogenously produced β-endorphin and met-enkephalin exert a physiological inhibition on luteinizing hormone-releasing hormone (LHRH) release in the central nervous system of sheep. Twenty-two mature ewes were implanted with unilateral guide tubes, through which matched infusion cannulae could be inserted without discomfort once daily for intracerebral (i.e.) infusion of three anti-opioid treatments: naloxone (50 µg in 20 µl), sheep antisheep β-endorphin (ABE; 20 µl of 1:25) or sheep anti-met-enkephalin (AME; 20 µl of 1:25) and of two control treatments: nonimmune sheep serum (20 µl of 1:25) or sheep antiporcine thyroglobulin (20 µl of 1:25). To detect abrupt disinhibition of LHRH release by anti-opioid treatments, serum luteinizing hormone (LH) was quantified at 10-min intervals for 1–2 h before and after each i.e. infusion. Complete trials consisted of 3–4 different anti-opioid or control i.e. infusions once daily at a single site over a period of 2–3 days during the luteal phase of recurring estrous cycles. Results were statistically evaluated within each ewe since complete trials were replicated 2–5 times within each ewe and because no 2 ewes could have i.e. infusions in identical locations. Anatomical generalizations were possible when LH responses to anti-opioid treatments were similar for several ewes with i.e. infusion sites in comparable brain regions. However, it was not possible to make such generalizations when infusion sites were not comparable in other ewes. In summary, naloxone consistently disinhibited LHRH/LH when infused into the mediobasal hypothalamus (n = 3), the anterior hypothalamic area (n = 4), the preoptic area (POA; n = 5) and the basal forebrain (BF; n = 5). Intracerebral immunoneutralization of β-endorphin with ABE disinhibited LHRH/LH release when infusions were into the rostral POA/nucleus accumbens region (n = 5) or into the anterolateral hypothalamus (n= 1). Infusions of ABE did not alter LH concentrations when administered into the BF(n = 7) or into areas of the hypothalamus other than the POA (n = 9). Intracerebral immunoneutralization of met-enkephalin with AME was not effective at any ABE-responsive sites (n = 6) or in the BF (n = 5), but it abruptly stimulated LHRH/LH release when infusions were into the anterior hypothalamic area (n = 2) or into the mediobasal hypothalamus (n = 1). Control infusions of antithyroglobulin serum did not alter patterns of serum LH concentrations. In summary, unilateral i.e. immunoneutralization of endogenous β-endorphin and of met-enkephalin in selected brain areas relieved the inhibition of LHRH release in luteal phase ewes. It is concluded that these two endogenous opioid peptides are involved in the physiological regulation of LHRH/LH release in the luteal phase ewe, and that they act at different sites of the centr

ISSN:0028-3835    

DOI:10.1159/000125609

出版商:S. Karger AG    

年代:1990

数据来源: Karger

摘要:

The aim of the present study was to evaluate the physiological significance of the rapid, short-loop, negative feedback of prolactin by passive immunization with antiserum to rat prolactin injected into the third cerebral ventricle (3 V) of conscious, freely moving intact or castrated male rats. Blood samples for measurement of plasma prolactin concentrations were removed through implanted external jugular catheters. After injection of 3 µl of undiluted antiserum, plasma levels of prolactin decreased rapidly (within 5 min) to values undetectable by RIA. Further study revealed that this dose of antiprolactin serum had combined with circulating prolactin, thus rendering it undectable by RIA. To overcome this problem, we repeated the experiment injecting 2 µl of diluted antiserum (dilution factors 20, 100, 200, 2,000) into the 3 V. When compared to values of plasma prolactin in control rats injected with 2 µl of normal rabbit serum, none of the dilutions of antiserum induced a significant change in prolactin concentrations for as long as 4 h after injection. Since there was no effect of intraventricularly injected antiprolactin serum on basal prolactin secretion, in the next experiment, intact as well as castrated male rats were subjected to ether stress 30 min after intraventricular injection of antiserum (dilution factor 100). The elevation of plasma prolactin which followed ether stress was significantly higher in male rats pretreated with antiprolactin serum than that which occurred in control rats. A similar enhancement of the increase in plasma prolactin following ether stress, but of longer duration, was obtained in castrated rats injected with antiprolactin serum. The results indicate that the rapid, negative short-loop feedback of prolactin attenuates stress-induced prolactin release. By contrast, there was no effect of the intraventricularly injected prolactin antiserum on plasma LH concentrations of the castrated mal

ISSN:0028-3835    

DOI:10.1159/000125610

出版商:S. Karger AG    

年代:1990

数据来源: Karger

摘要:

α-Methyl-p-tyrosine (α-MT), a competitive inhibitor of tyrosine hydroxylase, was used to block the synthesis of hypothalamic catecholamines in immature female rats of 14, 16 and 30 days of age and in castrated adults. The administration of α-MT (300 mg/kg body weight, free base) induced a significant decay in the hypothalamic content of norepinephrine (NE) and dopamine (DA) within the first 120 min. A second dose (150 mg/kg body weight), given 2 h after the first injection, did not further modify the low catecholamine levels observed 120 min after the first α-MT administration. The administration of 300 mg/kg body weight of α-MT induced a significant increase in LH concentrations in rats aged 14 and 16 days. On the contrary, after an α-MT injection, a significant LH decrease was observed in 30-day-old and in adult castrated rats. α-MT also increased FSH levels in prepubertal rats of 16 days of age, but no change occurred in 30-day-old and in adult rats. The administration of estrogen-progesterone (EP) to prepubertal rats of 16 days of age induced a significant decrease in serum LH levels as well as in the serotonin (5-HT) and 5-hydroxyindole-acetic acid (5-HIAA) concentrations in the anterior-preoptic hypothalamic area (AH-POA), but not in the medial basal hypothalamus. No modifications in the catecholamine content of these hypothalamic areas were observed in this age group after EP administration. On the contrary, in 30-day-old rats, EP induced a significant LH release as well as an increase in AH-POA concentrations of 5-HT, 5-HIAA and catecholamines. These data show that, during sexual development in the female rat, (1) the effect of catecholamines on LHRH-LH secretion changes from inhibition to stimulation, and (2) the modification in the feedback effects exerted by EP on LH is also accompanied by a changing effect of the ovarian hormones on catecholaminergic and serotoninergic systems. On this basis, the possibility exists that sexual maturation and the onset of puberty in the female rat involve the development of qualitatively different mechanisms of gonadotrophin control through changes in the ovarian hormones-neurotransmitters-LHRH interrelatio

ISSN:0028-3835    

DOI:10.1159/000125611

出版商:S. Karger AG    

年代:1990

数据来源: Karger

摘要:

Opioid peptides are present in both the posterior pituitary (PP) and stalk-median eminence (SME). Their effects on the dopaminergic neurons in the SME are well documented, but little is known concerning their role in the regulation of dopamine (DA) release from the PP. The objectives of this study were (1) to develop an in vitro method suitable for examining the regulation of endogenous DA release from PP and SME, and (2) to describe and compare the effects of selected opioid peptides on potassium-evoked DA release from these tissues. Tissues were dissected from ovariectomized rats and incubated in media. After equilibration, two pulses of 28 mM potassium (K+), 3 min each, were delivered 30 min apart. Test substances were administered 20 min before the second K+ stimulus. DA in the media was determined by high-performance liquid chromatography. Potassium at 28 and 56 mM elicited a marked increase in DA release from the PP and SME; this was abolished by the removal of calcium. The opioid receptor antagonist, naloxone, significantly increased the release of DA from both PP and SME by 55%. Dynorphin A elicited a significant inhibition of DA release from PP and SME by 33 and 50%, respectively. In contrast, methionine enkephalinamide decreased DA release from the SME by 50%, but was without effect in the PP. The release of DA from both PP and SME was significantly inhibited by β-endorphin, and this was reversed by naloxone. However, β-endorphin was fourfold more effective in the SME. N-acetyl-β-endorphin did not alter DA release. Conclusions: (1) we have developed a simple and sensitive in vitro method for studying the effects of hormones and drugs on the release of endogenous DA from PP and SME; (2) tuberoinfundibular dopaminergic and tuberohypophyseal dopaminergic nerve terminals are subjected to a similar inhibitory control by endogenous opioid peptides, and (3) exogenously applied opioid peptides exert differential effects on the release of DA from SME and PP which could be attributable to a dissimilar distribution of opioid receptor subtypes in these two tissu

ISSN:0028-3835    

DOI:10.1159/000125612

出版商:S. Karger AG    

年代:1990

数据来源: Karger

摘要:

Swimming at 25–30 °C for 30 min stimulates release of β-endorphin from both the anterior and intermediate lobe of the pituitary in rats. Measurement of N-acetyl β-endorphin-immunoreactivity (IR), which is specific for intermediate lobe secretion, indicates a 2- to 3-fold increase in N-acetyl β-endorphin IR in plasma following this challenge. When swim is repeated on a daily basis, there is an increase in the amount of N-acetyl β-endorphin IR released with repeated swim over time. As well as increased response to the swim challenge, these animals demonstrate an increase in the resting plasma levels of N-acetyl β-endorphin IR and an increase in the intermediate lobe content of N-acetyl β-endorphin IR. Molecular sieving of plasma from rats which were swum repeatedly demonstrates that this N-acetyl β-endorphin IR consists of both larger molecular weight N-acetyl β-endorphin IR, e.g. N-acetyl β-endorphinι_3i and C-terminally shortened forms, e.g. N-acetyl β-endorphin1–27- Administration of propranolol (3 mg/ kg), a β-adrenergic antagonist, 30 min before the onset of swim is able to block the intermediate lobe release of N-acetyl β-endorphin IR with acute swim challenge. However, repeated administration of propranolol in conjunction with repeated swim is not able to block the swim stress-induced increase in plasma N-acetyl β-endorphin IR or the increase in N-acetyl β-endorphin IR content of the intermediate lobe. This is not due to decreased sensitivity to propranolol with repeated administration since in rats given chronic propranolol treatment an acute dose of propranolol is still able to block swim stress-induced release of N-acetyl β-endorphin IR. Similarly, it is not due to a decreased efficacy of this dose of propranolol in rats which w

ISSN:0028-3835    

DOI:10.1159/000125613

出版商:S. Karger AG    

年代:1990

数据来源: Karger

ISSN:0028-3835    

DOI:10.1159/000125621

出版商:S. Karger AG    

年代:1990

数据来源: Karger