Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P01189 (beta-endorphin)
 21,003 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Hyperprolactinemia can reduce the LH secretion in rats, but the mechanism of the effect of PRL is not clear. We have investigated the actions of PRL on the secretion of LHRH and LH and the interaction among PRL, beta-endorphin (beta-EP), and LHRH. The effects of PRL on LHRH and LH secretion were studied in ovariectomized female rats after transplanting four anterior pituitaries to the right kidney capsule of each ovariectomized rat for 2-3 weeks. The level of PRL in rats with pituitary transplants was approximately 5 times higher than that in control rats. The concentration of LHRH in pituitary portal plasma of hyperprolactinemic rats was approximately 4 times lower than that in control rats. Hyperprolactinemic animals also showed lower plasma LH levels than the controls. Since beta-EP inhibits the secretion of LHRH, we have tested whether the reduced secretion of LHRH in hyperprolactinemic ovariectomized rats is associated with an increase in beta-EP activity. This was studied by measuring the concentration of beta-EP in pituitary portal plasma and the response of LHRH and LH to the opiate antagonist naloxone. The level of beta-EP-like immunoreactivity in pituitary portal plasma was significantly higher in hyperprolactinemic rats than in control animals. Naloxone (10 mg/kg, sc) increased both LHRH and LH concentrations in hyperprolactinemic rats, but not in control rats. The present results demonstrate that hyperprolactinemia can reduce LHRH release and suggest a possible involvement of beta-EP in the PRL inhibitory action on LHRH.
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PMID:Hyperprolactinemia decreases the luteinizing hormone-releasing hormone concentration in pituitary portal plasma: a possible role for beta-endorphin as a mediator. 315 64

Male golden hamsters were exposed to long photoperiod or short photoperiod (SP) and injected with 1 microgram TRH and/or 1 microgram LHRH at lights on (LO) or lights off (LX) for a total of 8 weeks. Both TRH and LHRH prevented testicular regression if they were injected at LO. Injected at LX, TRH did not prevent testicular regression, and LHRH was only partially effective. Plasma beta-endorphin levels were significantly higher in groups with atrophic testes. These results indicate that TRH like LHRH can prevent SP-induced testicular regression in hamsters by some unknown mechanism and that beta-endorphin may be involved in the control of testicular function in hamsters.
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PMID:Temporal difference of thyrotropin-releasing hormone in prevention of testicular regression in golden hamsters exposed to short photoperiods: possible involvement of beta-endorphin. 315 80

This study examines the possible involvement of beta-endorphin in the photoperiodic control of reproduction in the Syrian hamster. beta-Endorphin and LHRH concentrations in the medial basal hypothalamus (MBH), anterior hypothalamus (AHA), and the preoptic area (POA) as well as pineal melatonin content were determined by RIA in male Syrian hamsters exposed to either a long day [(LD) 16-h light; 8-h dark; lights on 0700-2300] or short day [(SD) 8-h light, 16-h dark; lights on 0700-1500] for 8 weeks. Groups of eight animals from each photoperiod were killed by decapitation at 4-h intervals over 24 h. Twenty minutes before death half the animals from each photoperiod were given naloxone (5 mg/kg, sc), the other half saline. Exposure to a long photoperiod maintained testicular activity while a short photoperiod induced testicular regression. Pineal melatonin content in both photoperiods was maximal at 0500 h, i.e. 2 h before the onset of light (SD, 435.58 +/- 82.7 pg/pineal; LD, 276.78 +/- 56.8 pg/pineal). However, the duration of the nighttime rise in pineal melatonin content was increased in SD animals with elevated melatonin levels at 2100 h (157.10 +/- 41.8 pg/pineal) and 0100 h (199.11 +/- 58.9 pg/pineal). In contrast pineal melatonin content in LD animals was only higher than daytime values at 0500 h. A daily rhythm of beta-endorphin content within both the AHA and MBH of animals exposed to a short photoperiod coincided with this prolonged nighttime rise in pineal melatonin content, although a causal relationship between the two was not established. Peak levels of beta-endorphin occurred at 2100 h (AHA, 6.569 +/- 1.2 pmol/mg protein; MBH, 4.877 +/- 0.45 pmol/mg protein) and at 0100 h (AHA, 6.107 +/- 0.66 pmol/mg protein; MBH, 4.49 +/- 00.79 pmol/mg protein) which was 6 h and 10 h into the dark phase, respectively, with lowest levels in the middle of the light phase (AHA, 3.561 +/- 0.56 pmol/mg protein; MBH, 2.688 +/- 0.3 pmol/mg protein). This rhythm was absent in animals exposed to a long photoperiod. There was no effect of photoperiod or time of day on the content of beta-endorphin in the POA. LHRH levels were not altered by changes in photoperiod in all three brain regions studied. In the AHA and MBH, concentrations of LHRH were similar at all times of day whereas, in the POA, LHRH levels varied with time in both photoperiods. Peak levels occurred in the middle of the dark phase at 0100 h (LD, 2.774 +/- 0.24 pmol LHRH/mg protein; SD, 3.206 +/- 0.48 pmol LHRH/mg protein) with lowest levels during the light phase (LD, 1.664 pmol LHRH/mg protein; SD, 1.775 pmol LHRH/mg protein).(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Changes in photoperiod alter the daily rhythms of pineal melatonin content and hypothalamic beta-endorphin content and the luteinizing hormone response to naloxone in the male Syrian hamster. 315 63

We examined the effects of intraventricular (Ivt) administration of beta-endorphin (beta E) on preovulatory LH release, ovulation, and the mechanism that may be involved in opioid action. Female rats were implanted with permanent cannulae in the third ventricle of the brain and were allowed to recover 4-day estrous cyclicity. Intrajugular cannulae were placed on the morning of proestrus. Thereafter, they received Ivt either saline (2 microliter) or beta E (10 micrograms/2 microliter) at 1300, 1430, and 1600 h. In addition, at 1600, 1700, and 1800 h, they were injected Ivt with either vehicle (cerebrospinal fluid or saline) or one of the following compounds: epinephrine (15.3 micrograms), norepinephrine (15.3 micrograms), or prostaglandin E2 (6 micrograms). Blood samples for LH measurements were taken 0, 10, 30, and 60 min after the additional injections at 1600 and 1700 h. beta E blocked the preovulatory LH surge and ovulation. Administration of the opiate receptor antagonist naloxone (2 mg/kg) reversed these effects. Epinephrine stimulated a small discharge of LH only after a second E injection in the beta E-treated rats, but this was insufficient to restore ovulation. On the other hand, prostaglandin E2 reversed the beta E blockade of the LH surge and ovulation. These studies suggest that beta E blocks ovulation and the LH surge primarily by suppressing either the influx or adrenergic expression of the spontaneous neurogenic stimuli responsible for the preovulatory LH discharge and not by evoking a general decrease in the secretory response of the LHRH neurons.
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PMID:Reversal of beta-endorphin-induced blockade of ovulation and luteinizing hormone surge with prostaglandin E2. 316 May 73

Gonadal, adrenal, and thyroid functions were evaluated in 70 men seropositive for human immunodeficiency virus (HIV) infection, clinically categorized as asymptomatic (n = 19), AIDS-related complex (ARC) (n = 9), or acquired immunodeficiency syndrome (AIDS) (n = 42). Twenty of 40 men (50 percent) with AIDS were hypogonadal. Mean serum testosterone concentrations in both ARC (292 +/- 70 ng/dl) and AIDS (401 +/- 30 ng/dl) men were significantly less than in asymptomatic (567 +/- 49 ng/dl) or normal men (608 +/- 121 ng/dl). Of these hypogonadal men, 18 of 24 (75 percent) had hypogonadotropic hypogonadism. Seven of eight hypogonadal men (88 percent) had a normal gonadotropin response to gonadotropin-releasing hormone administration. Hypogonadism correlated with lymphocyte depletion and weight loss. Adrenal cortisol reserve, evaluated by adrenocorticotropin stimulation, was normal in 36 of 39 patients (92 percent) with AIDS. Indices of thyroid function were normal with the exception of one ARC man with a low free thyroxine index. In conclusion, hypogonadism is common in men with HIV infection and may be the first or most sensitive endocrine abnormality.
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PMID:Endocrine disorders in men infected with human immunodeficiency virus. 334 69

Membrane currents of identified, isolated corticotropes and gonadotropes from mammalian anterior pituitary gland have been evaluated. Pituitary gonadotropes and corticotropes were isolated enzymatically and stained in the living state using biotinylated gonadotropin-releasing hormone (Bio-GnRH) or biotinylated corticotropin-releasing hormone (Bio-CRF) followed by avidin fluorescein. Electrophysiological recordings were made with patch-clamp electrodes in the whole-cell clamp configuration. Tetrodotoxin (TTX)-sensitive sodium currents were larger in corticotropes than in gonadotropes. Corticotropes showed two components of calcium currents, a transient low-threshold component and a longer lasting high-threshold component. Small TTX-resistant inward currents were present also in gonadotropes, and both cell types had transient and steady potassium currents.
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PMID:Membrane currents of identified isolated rat corticotropes and gonadotropes. 354 30

Centrally administered neuropeptides were investigated for their effects on the development of gastric lesions in rats. Thyrotropin releasing hormone (TRH), vasoactive intestinal peptide (VIP) and gonadotropin releasing hormone (LHRH) produced gastric lesions acutely, with TRH demonstrating the most pronounced effect in terms of incidence and severity. Ten-fold higher doses of the same peptides administered intravenously produced none or very few gastric lesions. Moreover, pretreatment with atropine partially inhibited their production. Corticotropin releasing factor (CRF) exhibited only mild ulcerogenic effects, and the gastric lesions induced with this peptide developed more slowly than with TRH, VIP and LHRH. Although ulcerogenic in their own right, none of these four neuropeptides significantly potentiated the potent ulcerogenic effects of cold-restraint stress. Since other neuropeptides, including somatostatin, human pancreatic growth hormone releasing factor (hpGRF), substance P, bombesin, and neurotensin, had no demonstrable effects on gastric mucosa, we can conclude that the lesions were not a general effect of intracisternal administration of neuropeptides. The results suggest that within the central nervous system, there are several neuropeptides that play a significant role in the development of gastric lesions via, at least in part, vagal-dependent mechanisms.
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PMID:The effects of centrally administered neuropeptides on the development of gastric lesions in the rat. 392 Apr 62

A growing body of evidence suggests that neural peptides may induce important modulations on vegative and motor functions of the eye. The present study was designed to evaluate the effect of intracameral (I.C.) administration of alpha-melanocyte-stimulating hormone (alpha-MSH) and several other ocular peptides on intraocular pressure (IOP) in rabbits. alpha-MSH (5 micrograms) produced a significant and prolonged unilateral increase of IOP. This effect of I.C. alpha-MSH was dose-dependent (ED50 = 2.5 micrograms). Structure-activity studies revealed that equimolar doses of beta-MSH and gamma-MSH, unlike alpha-MSH, were totally ineffective. In addition, the structurally unrelated peptides beta-endorphin, thyrotropin-releasing hormone (TRH) and gonadotropin-releasing hormone (Gn-RH) did not affect IOP, when tested in a dose equimolar to 5 micrograms of alpha-MSH. These results confirm and extend previous observations, suggesting that alpha-MSH may be an important factor involved in regulation of IOP.
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PMID:Intracameral administration of alpha-MSH increases intraocular pressure in rabbits. 408 Jan 14

The pars distalis of the avian adenohypophysis consists of well-defined cephalic and caudal lobes which are distinct in their cellular constituents. Immunocytochemical investigations on the pituitary hormones of the pars distalis of the Japanese quail reveal five types of secretory cells, adenocorticotropin (ACTH) cells, prolactin (PRL) cells, thyroid-stimulating hormone (TSH) cells, growth hormone GH (STH) cells, and FSH/LH (gonadotropic) cells. The ACTH cells, TSH cells, and PRL cells are restricted to the cephalic lobe, and GH (STH) cells are confined to the caudal lobe, while FSH/LH cells are distributed throughout the cephalic and caudal lobes. The median eminence of birds has distinct anterior and posterior divisions, each with different neuronal components. The avian hypophysial portal vessels also consists of two groups, anterior and posterior. The peculiar arrangement and distribution of the avian hypophysial portal vessels are possibly related to the distribution of neuropeptides in the two divisions of the median eminence and to the cytological and functional differentiation of two lobes of the pars distalis. The localization of perikarya and fibers containing luteinizing hormone releasing hormone (LHRH), somatostatin, vasotocin, mesotocin, corticotropin-releasing factor (CRF), vasoactive intestinal polypeptide (VIP), glucagon, metenkephalin, and substance P in the hypothalamus and median eminence of the Japanese quail has been investigated by means of immunohistochemistry using antisera against the respective neuropeptides. LHRH-, somatostatin-, VIP-, met-enkephalin-, and substance P-immunoreactive fibers are localized in the external layer of the anterior and posterior divisions of the median eminence, while CRF- and vasotocin-reactive fibers are demonstrated only in the external layer of the anterior division of the median eminence. The metenkephalin fibers are thicker in the anterior median eminence but the substance P fibers are more abundant in the posterior division. Mesotocin fibers occur only in the internal layer of the median eminence and neural lobe.
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PMID:Immunohistochemistry of the hypothalamic neuropeptides and anterior pituitary cells in the Japanese quail. 608 43

Levels of immunoreactive beta-endorphin and luteinizing hormone releasing hormone (LHRH) were measured in brain tissue of aged male Long-Evans rats. The animals were tested for sex behavior twice in one week at bimonthly intervals between the 7th and 27th month of life and were sacrificed along with a group of young (5-month old) sexually active rats. Thirty-one of the 89 rats which began the study remained healthy and tumor-free. By month 27, 21 of these had completely ceased to mate and 10 continued to show adequate sexual behavior. Diminished levels of beta-endorphin-like immunoreactivity were measured in the hypothalami and hindbrain of the old animals grouped together as compared to young animals and this reduction was shown to be significantly greater in hypothalamic tissue from the behaviorally inactive subgroup. Hypothalamic LHRH levels were not significantly altered by age in these animals. However, a marked reduction of LHRH content in the septal and midbrain regions of the aged-behaviorally inactive subgroup was evident when compared with the behaviorally active group. The data suggest that altered function of beta-endorphin and LHRH neurons of the aged brain may be involved in the behavioral deterioration observed in aged animals.
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PMID:Immunoreactive-beta-endorphin and LHRH levels in the brains of aged male rats with impaired sex behavior. 609 83


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