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)

Thyrotropin-releasing hormone (TRH) immunoreactivity was localized in the rat anterior pituitary with rabbit anti-TRH sera and the unlabeled antibody peroxidase-antiperoxidase complex (PAP) technique. Stain was present in secretory granules of cells possessing morphological characteristics of thyrotropes, gonadotropes and lactotropes. Antibody absorption studies with anti-TRH sera absorbed with TRH, 3 diastereoisomeric analogues of TRH, gonadotropin-releasing hormone (GnRH), bovine serum albumin, thyrotropin, prolactin, adrenocorticotropin, luteinizing hormone, follicle stimulating hormone were performed to determine the specificity of the staining reaction. Only absorption with TRH resulted in a significant reduction in staining intensity. In vitro experiments were then begun with hemipituitaries to ascertain if intrapituitary TRH might originate by sequestration of exogenous, plasma membrane bound TRH or by de novo synthesis. The results suggest that anterior pituitary TRH is of endogenous origin.
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PMID:Endogenous thyrotropin-releasing hormone in the anterior pituitary: sites of activity as identified by immunocytochemical staining. 8 70

Thyrotropin-releasing hormone (TRH) has been reported to stimulate the release of melanocyte-stimulating hormone (MSH) from the pars intermedia (PI) of Rana esculenta. To test its effect on the rat PI, acutely dispersed rat PI cells, as well as whole nervosa-intermedias (NI), were incubated with synthetic TRH, from 10(--10)--10(--4)M. TRH did not alter the release of either MSH or adrenocorticotropic hormone (ACTH).
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PMID:Thyrotropin-releasing hormone does not alter the release of melanocyte-stimulating hormone or adrenocorticotropic hormone from the rat pars intermedia. 20 81

Thyrotropin-releasing hormone (TRH) is a potent stimulator of melanotropin (alpha-MSH) release from pituitary melanotrophs in pig, frog, and fish. Concurrently, it has recently been shown that injection of TRH induces skin darkening in the lizard Anolis carolinensis (Licht and Denver, 1988). In the present study, we have thus investigated in vitro the possible effect of TRH on alpha-MSH release from the lizard (Lacerta vivipara) neurointermediate lobe, by means of the perifusion technique. Using our radioimmunoassay procedure, we found that serial dilutions of L. vivipara NIL extracts and synthetic alpha-MSH gave parallel binding curves. Administration of graded doses of TRH (10(-8)-10(-6) M) did not cause any modification of alpha-MSH release. In contrast, infusion of a depolarizing concentration of K+ induced a robust stimulation of alpha-MSH secretion. These results indicate that, in the lizard L. vivipara, the neuropeptide TRH does not stimulate pituitary melanotrophs.
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PMID:Lack of effect of TRH on alpha-MSH release from the neurointermediate lobe of the lizard Lacerta vivipara. 139 12

Thyrotropin-releasing hormone (TRH), ovine corticotropin-releasing hormone (oCRH) (both 268 nM), and mammalian gonadotropin-releasing hormone (mGnRH) (268 and 2680 nM) stimulated the secretion of bioactive thyrotropin (TSH) by Rana esculenta pituitaries (pars distalis) in vitro. Preincubation of the pituitaries with 50 ng/ml (64 nM) thyroxine (T4) for 6 hr suppressed the TRH- and oCRH-induced (268 nM) secretion of bioactive TSH, but did not affect the response of the pituitaries to 268 nM mGnRH. Triiodothyronine (T3) (64 nM) reduced both the TRH- and mGnRH-stimulated release of bioactive TSH; the response of TSH to TRH even decreased toward basal levels while a significant TSH response to mGnRH remained. In a separate experiment, pituitaries were preincubated for 6 hr with different equimolar doses of T3 and T4 (6.4, 32, and 64 nM); neither treatment affected the mGnRH-stimulated secretion of bioactive TSH. On the other hand, T4 suppressed the TSH response to TRH in a dose-dependent manner. The inhibitory effects of thyroid hormones on the TRH-induced release of bioactive TSH was present for at least 4 hr after their removal from the incubation medium. These results suggest that thyroid hormones exert a negative feedback control on the secretion of bioactive TSH in adult frogs by a direct action on the pars distalis. There may also be differences in thyroid hormone sensitivities of the TSH responses to mGnRH and TRH.
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PMID:Thyroid hormone feedback regulation of the secretion of bioactive thyrotropin in the frog. 149 May 87

Several of the non-sex hormones have been found to be useful in the treatment of seizures. These hormones have an effect on seizures, and seizures have an effect on these hormones. Adrenocorticotropic hormone (ACTH) and corticosteroid drugs have been found to be useful in the treatment of infantile spasms and other seizure disorders. Unfortunately, there is no clear consensus regarding superiority of ACTH versus prednisone in regard to efficacy and long-term benefits, dosage, or duration of treatment. There is also considerable debate regarding reasons why ACTH and prednisone are useful in infantile spasms, their mechanism of action, and their long-term effects on brain development. Thyrotropin-releasing hormone also has been used in the treatment of infantile spasms and other seizure types in children, with modest success. As with ACTH and prednisone, the mechanisms of action remain unclear.
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PMID:Effect of non-sex hormones on neuronal excitability, seizures, and the electroencephalogram. 165 81

The localization of thyrotropin-releasing hormone-immunoreactive structures was investigated in the hypothalamo-hypophyseal complex of the frog, Rana ridibunda, by light and electron microscopy using the conventional indirect immunoperoxidase technique and the immuno-gold technique, respectively. The localization of mesotocin-, vasotocin- and neurophysin-immunoreactive elements was compared to that of thyrotropin-releasing hormone either by comparing homologous fields on serial sections or by staining the same section with two different antibodies. Thyrotropin-releasing hormone-immunoreactive perikarya occurred mainly in the anterobasal periventricular area and dorsal extension of the preoptic nucleus, and in the lateral zone of the infundibular nucleus. In the anterobasal preoptic nucleus, the distribution of thyrotropin-releasing hormone-immunoreactive perikarya partially overlapped that of vasotocin- and mesotocin-containing neurons; however, co-localization of thyrotropin-releasing hormone with either nonapeptide could not be detected there. In contrast, in the caudal extension of the preoptic nucleus, thyrotropin-releasing hormone- and mesotocin-like immunoreactivities were frequently co-localized in the same neurons. In the external zone of the median eminence, abundant networks of thyrotropin-releasing hormone- and vasotocin-immunoreactive nerve fibers were found in the vicinity of portal capillaries, while mesotocin-immunoreactive axons were only found in the internal zone. Using the immuno-gold technique at the electron microscopic level, three distinct thyrotropin-releasing hormone-immunoreactive systems were identified in the median eminence-neurointermediate lobe complex. (1) In the external zone of the median eminence, a conspicuous population of pericapillary endings contained 100-nm dense core vesicles immunoreactive solely for thyrotropin-releasing hormone. (2) In the neural lobe of the pituitary, thyrotropin-releasing hormone immunoreactivity occurred on secretory vesicles in a subpopulation of the mesotocinergic axons containing 160-nm secretory granules; co-localization with vasotocin was never seen. (3) In the intermediate lobe, thyrotropin-releasing hormone- and mesotocin (or neurophysin I)-immunoreactivities were systematically found in the same 120-nm dense core vesicles; these thyrotropin-releasing hormone-/mesotocin-immunoreactive axon terminals frequently made synaptic contacts with melanotropic cells. The possible modulatory effect of mesotocin on thyrotropin-releasing hormone-induced alpha-melanocyte-stimulating hormone secretion was investigated using perifused frog neurointermediate lobes. Administration of graded doses of mesotocin (from 10(-10) to 10(-5) M) did not affect the spontaneous release of alpha-melanocyte-stimulating hormone. In addition, mesotocin (10(-7) and 10(-6) M) did not modify thyrotropin-releasing hormone-evoked alpha-melanocyte-stimulating hormone release.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Three distinct thyrotropin-releasing hormone-immunoreactive axonal systems project in the median eminence-pituitary complex of the frog Rana ridibunda. Immunocytochemical evidence for co-localization of thyrotropin-releasing hormone and mesotocin in fibers innervating pars intermedia cells. 251 4

Thyroliberin produces a marked depressant action on the reflex cerebrovascular constriction reactions. The lack of changes in the content of immunoreactive beta-endorphine in blood and CSF indicates that apparently the cerebrovascular effects of the drug are not mediated via the opioid system but are due to a direct influence of thyroliberin on the central mechanisms by which brain circulation is regulated. Thyroliberin increases the blood corticotropin content, which causes an elevation of the arterial blood pressure and cerebrovascular tension. On the contrary, in the CSF the corticotropin level decreases after thyroliberin administration. The data obtained show that there is no correlation between the content of beta-endorphine and corticotropin in blood and CSF under the action of thyroliberin.
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PMID:[Brain blood supply and beta-endorphin and corticotropin content on exposure to thyroliberin]. 298 50

Development of the DMBA-induced breast cancer in rats resulted in an increase of the thyrotropin, somatotropin and prolactin concentrations in blood plasma. Thyroliberin (TRH) stimulation of the thyrotropin secretion was decreased. Basal levels of the corticotropin (ACTH) and lutropin (LH) as well as of the luliberin (LRH) stimulation of the LH secretion were not changed. Concentrations of estradiol, corticosterone and insulin enhanced, those of testosterone, progesterone and thyroxine lowered. Out of two calcitropic hormones, RTH and CT, the secretion of the latter increased.
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PMID:[Plasma hormone levels in rats with DMBA-induced mammary tumors]. 609 41

The effects of intracerebroventricular administration of several peptides on discrete-trial, conditioned avoidance responding were assessed in the rat. Three peptides (neurotensin, bombesin and beta-endorphin) produced a neuroleptic-like effect (i.e. a decrease in avoidance responding with no effect on escape responding). A low dose (0.6 nmol) of each peptide elicited a significant effect. Neurotensin and bombesin produced a significant but partial decrease in avoidance responding; larger doses of these peptides did not produce a greater effect. beta-Endorphin elicited dose-related decrements in avoidance responding. In addition, the effect of neurotensin, but not bombesin or beta-endorphin, was antagonized by simultaneous administration of an equimolar dose of thyrotropin-releasing hormone. Hence, the 3 peptides do not appear to produce decreases in avoidance responding by the same mechanism. Thyrotropin-releasing hormone, luteinizing hormone-releasing hormone, bradykinin, substance P, des-Tyr1-gamma-endorphin and melanotropin inhibiting factor did not significantly affect avoidance responding. These findings, taken together with previous findings, suggest that intracerebroventricular administration of certain endogenous peptides (neurotensin, bombesin and beta-endorphin) may exert neuroleptic-like effects.
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PMID:The effects of neuropeptides on discrete-trial conditioned avoidance responding. 617 91

The oligopeptides were microiontophoretically applied to neurons of the sensory cortex, hippocampus, thalamus and septum. Metenkephalin and beta-endorphin increased activity of some neurons while decreasing it in other cells. Nalorphine antagonized the inhibition effect of metenkephalin in all the brain areas under study. Inhibition of the peptide activating action occurred in hippocampal and septal neurons. A correlation between effects of metenkephalin and beta-endorphin on the same neurons was revealed in the cortex and thalamus. Thyroliberin mostly activated neurons in all the areas. Independence of neuronal effects of TRH and opioid peptides was obvious.
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PMID:[Sensitivity of neurons in different regions of the brain to met-enkephalin, beta-endorphin, and thyroliberin in the rat]. 626 11


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