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)

The central nervous system effects of neuropeptides on gastric acid and duodenal bicarbonate secretions were examined. In freely moving rats, i.c.v. administration of thyrotropin-releasing hormone (TRH), human gastrin-17 (hG-17) and the somatostatin analogue, desAA 1,2,4,5,12,13 [D-Trp8]somatostatin (ODT8-SS), significantly increased gastric acid secretion, while vasoactive intestinal peptide (VIP) had no effect. In the order of potency and efficacy, the following peptides decreased acid secretion: bombesin (BOM) greater than calcitonin gene-related peptide (CGRP) greater than calcitonin (CT) greater than corticotropin-releasing factor (CRF) greater than beta-endorphin (beta-END) greater than neurotensin (NT). In anesthetized rats, none of these peptides significantly altered proximal duodenal bicarbonate secretion. In awake, freely moving rats, cerebroventricular administration of CGRP significantly decreased while ODT8-SS, TRH and CRF significantly increased duodenal bicarbonate secretion. beta-Endorphin, VIP, CT, BOM, NT and hG-17 given i.c.v. did not significantly alter the bicarbonate response. These results indicate that neuropeptides administered into the central nervous system modulate gastric acid as well as duodenal bicarbonate secretions in awake, freely moving rats in a differentiated fashion. CGRP inhibits both acid and bicarbonate secretions, a somatostatin analogue and TRH both stimulate acid and bicarbonate secretions and CRF inhibits gastric acid but stimulates duodenal bicarbonate secretions.
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PMID:Effects of neuropeptides on gastric acid and duodenal bicarbonate secretions in freely moving rats. 271 Sep 63

Adenohypophysial cells from female Wistar rats were dispersed and maintained for 4 days in primary culture in the presence of [3H]myoinositol. The effects of several releasing hormones, corticotropin-releasing factor (CRF), arginine vasopressin (AVP), angiotensin II (A II), thyrotropin-releasing hormone (TRH), and luteinizing hormone-releasing hormone (LHRH) on the liberation of labelled inositol phosphate (InsP), inositol-bisphosphate (InsP2), and inositol-trisphosphate (InsP3) from prelabelled inositol lipids were tested alone and in combination. Of the corticotropin (ACTH) secretagogues tested, AVP and A II produced a dose-dependent increase in inositol phosphate accumulation. CRF was inactive. The ED50 values of about 1 nM for both AVP and A II were close to the corresponding dissociation constants for binding to pituitary membranes: and, in the case of A II, close to the ED50 for A II-induced inhibition of pituitary membrane adenylate cyclase. The responses to A II and AVP could be inhibited by [Sar1,Ile8]A II and the AVP antagonist d(Et2)-VAVP, respectively. The magnitude of the maximal effect of AVP on accumulation of inositol phosphates was small (25% increase over basal value) suggesting that this effect was restricted to a minor subpopulation of pituitary cells (probably corticotrophes). CRF did not potentiate AVP-induced inositol phosphates accumulation. Maximal A II-induced increase in inositol phosphates accumulation represented 150% of the basal value and was partially additive with that of TRH suggesting that lactotrophes represent the main A II-sensitive subpopulation.
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PMID:Vasopressin and angiotensin induce inositol lipid breakdown in rat adenohypophysial cells in primary culture. 282 20

Six normal and 8 neoplastic adrenal medullae were assayed for several immunoreactive (IR) proopiomelanocortin (POMC) and hypothalamic peptides. IR-POMC peptides were found in normal and tumor tissue in concentrations ranging from 0.0003 to 0.1% of those in pituitary. Their molecular sizes resembled those of pituitary intermediate lobe POMC peptides. No intact POMC was found. One pheochromocytoma contained fully bioactive IR-adrenocorticotropic hormone (IR-ACTH; Mr approximately 4,500) and an intermediate-sized (Mr approximately 10,000) IR-ACTH with approximately 69% bioactivity. Normal and tumorous medullae contained IR-corticotropin-releasing hormone (CRH) in concentrations ranging from 0.6 to 4% of those in hypothalamus except for one pheochromocytoma that contained 40 times that amount of IR-CRH, which was chromatographically indistinguishable from hypothalamic CRH and fully bioactive. IR-somatostatin and IR-growth hormone-releasing hormone were found in both tissue types, but IR-gonadotropin-releasing hormone and IR-thyrotropin-releasing hormone (TRH) were not, although IR-histidyl-proline diketopiperazine, a putative TRH metabolite, was found. IR-arginine vasopressin was found in two normal medullae, but not in pheochromocytomas.
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PMID:Pituitary and hypothalamic hormones in normal and neoplastic adrenal medullae: biologically active corticotropin-releasing hormone and corticotropin. 282 21

The motor functional recovery after sciatic nerve crush was measured in rats treated with daily injections of (a) thyrotropin-releasing hormone (2.0 mg/kg, (b) alpha-melanocyte-stimulating hormone (0.07 mg/kg/48 h), or (c) testosterone propionate (4.4 mg/kg). The recovery of the motor function of the sciatic nerve was indicated by using the return of the toe-spreading response. None of the treatments differed significantly from saline controls in the time needed for recovery. The same procedure (without injections) was carried out with castrated and noncastrated male rats in order to test the effect of the lack of testosterone on recovery time after sciatic crush. The groups did not differ significantly as to their recovery times. The same method was used to study the effect of spermine (10.0 mg/kg/day) on the recovery of motor function. Spermine seemed to reduce the time needed for recovery from a mean value of 15.7 to 11.0 days (P less than 0.01). We also studied the effect of daily injections of spermine (13.0 mg/kg) on the sensory division of the peripheral nerve using the foot-flick test. The time needed for recovery after crush in the sciatic notch was reduced from 13.7 to 7.7 days (P less than 0.005). These results do not support the hypothesis that alpha-melantocyte-stimulating hormone, thyrotropin-releasing hormone, or testosterone enhance functional recovery of severed motor axons. Our results confirm a previous observation that spermine reduces the time needed for recovery after trauma in peripheral motor neurons. The result of the foot-flick test suggests that spermine enhances both motor and sensory recovery.
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PMID:Putative stimulants for functional recovery after neural trauma: only spermine was effective. 282 13

The effects of several hypothalamic peptides on hormone secretion by pituitaries of three species of anuran amphibians were investigated using in vitro techniques. Secretion of thyrotropic bioactivity (designated thyrotropin or TSH) was quantified by bioassay of the pituitary incubation medium using thyroxine (T4) production by paired thyroids from the same animals. Pituitaries from adult male Rana pipiens were cultured in medium alone, 10 or 100 ng/ml thyrotropin-releasing hormone (TRH), 1000 ng/ml ovine corticotropin-releasing hormone (oCRH), or 300 ng/ml synthetic mammalian gonadotropin-releasing hormone (mGnRH) (these represent approximately equimolar doses) for two 2-hr incubation periods. TSH secretion by control glands was nondetectable, but glands exposed to TRH increased their secretion of TSH in a dose-dependent manner. Both oCRH and mGnRH also stimulated significant increases in TSH. oCRH produced greater output of TSH than did the other two peptides and mGnRH was less active than TRH. Secretion of immunoreactive gonadotropin (GtH) was increased by mGnRH, but not by the other two peptides. Pituitaries from two other anuran species, Hyla regilla and Xenopus laevis, also responded to 100 ng/ml TRH by releasing TSH. These results provide the first unequivocal evidence that TRH can act directly on the anuran amphibian pituitary to stimulate the secretion of TSH, and suggest that the presence of functional TRH receptors on pituitary thyrotropes may be of greater phylogenetic antiquity than has been assumed previously. Furthermore, these data suggest the potential for multihormonal control of TSH secretion in frogs.
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PMID:Several hypothalamic peptides stimulate in vitro thyrotropin secretion by pituitaries of anuran amphibians. 285 81

We have previously reported that intracameral (I.C.) administration of neurotensin (NT) potently induces a time- and dose-dependent miosis in rabbits. This study was designed to determine structure-function relationships for NT-induced miosis. NT and twelve different fragments and analogs of NT, and the structurally-unrelated peptides beta-endorphin (beta-end), somatostatin (SRIF) and thyrotropin-releasing hormone (TRH) were tested in a dose equimolar to 30 micrograms of NT for their effects on pupillary diameter (PD) in rabbits. In confirmation of previous findings, NT produced significant miosis. Followed in order of duration of effect were D-Trp11-NT, D-Tyr11-NT, the N-terminal fragment NT1-12, [Gln4] - NT and NMe-NT. The N-terminal fragment NT1-8, D-Arg8-NT, and D-Phe11-NT were weakly active. In addition, the initial N-terminal fragment NT1-6 and the C-terminal fragments NT8-13 and NT9-13 did not affect PD. D-Pro10-NT, beta-end, SRIF, and TRH were totally ineffective. The results of this investigation contribute to support a role for NT on regulation of pupillary function, and suggest that the midportion of NT appears to be critical for the expression of NT-induced miosis.
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PMID:Pupillary effects of neurotensin: structure-activity relationships. 286 86

Neuropeptides represent a new class of compounds with important implications for the understanding of the mechanisms and treatment of epileptic disorders. Several systems of peptide modulators--in particular the opioid-like peptides, vasopressin, somatostatin, thyrotropin-releasing hormone (TRH) and ACTH--have partially demonstrated endogenous roles in some forms of epilepsy. Seizures and stressful situations may release endogenous opioid peptides and mediate postictal depression and postictal seizure refractoriness. Vasopressin is believed to increase susceptibility to convulsions and may be involved in the pathogenesis of febrile convulsions. Derangements in TRH regulation may lower thresholds for seizure expression by regulating arousal systems; however, some TRH analogs have proven to be effective anticonvulsants. Long-term alterations in somatostatin regulation could be components of focal epilepsies. ACTH is particularly useful in the treatment of infantile spasms. Pharmacological effects of these and other peptides have potentials for defining new classes of anticonvulsants. Cholecystokinin (CCK) and its analogs, the opioid peptides beta-endorphin and FK33824, TRH analogs, and several dipeptides exhibit potent anticonvulsant properties in chemical, electroshock, and genetic model screens. Convulsant actions of CRF, somatostatin, TRH, vasopressin, and high doses of endorphin or enkephalins may provide new tools to study regulatory mechanisms of cerebral excitability. The enkephalin epileptogenic effect is being developed as a predictive tool for new anti-petit mal anticonvulsants. Advances in molecular biology have identified the genes of particular peptide families. A concept has developed that the large propeptide precursors, coded by these genes, whose processing leads to functional peptide formation and release, regulate peptidergic humoral responses to external stimuli. This idea may have particular application in the understanding of the genetic basis of some seizure states. Techniques for amplification of mRNA expression have identified specific neuronal proteins and peptides. Knowledge of protein and propeptide structural cleavage sites has suggested previously unknown candidates for modular systems in epileptic states. Technological advances in automated peptide sequencing and synthesis have allowed the development of metabolically resistant analogs and antagonist peptides. The anticonvulsant potencies of CCK, TRH, and opioid peptides have been defined more clearly with these methods.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Neuropeptides: anticonvulsant and convulsant mechanisms in epileptic model systems and in humans. 287 23

The anteroventral periventricular nucleus (AVPv), which lies in the periventricular zone of the preoptic region, is critical for normal phasic gonadotropin secretion since lesions of this nucleus abolish the progesterone-induced surge of luteinizing hormone secretion from the anterior pituitary, block ovulation, and induce persistent vaginal estrus in female rats. However, very little is known about the neurotransmitter-specific pathways associated with this nucleus. In the present study we evaluated the distribution of biochemically specific cells and fibers within the AVPv and adjacent regions by using an indirect immunohistochemical method with antisera to serotonin (5-HT), dopamine beta-hydroxylase (DBH), tyrosine hydroxylase (TH), neuropeptide Y (NPY), cholecystokinin-8 (CCK), vasoactive intestinal polypeptide (VIP), substance P (SP), neurotensin (NT), corticotropin-releasing factor (CRF), luteotropin-releasing hormone (LRH), somatostatin (SS), thyrotropin-releasing hormone (TRH), oxytocin (OXY), vasopressin (VAS), adrenocorticotropic hormone (ACTH1-24), alpha-melanocyte-stimulating hormone (alpha-MSH), leucine-enkephalin (L-ENK), and calcitonin gene-related peptide (CGRP). Our findings indicate that both cells and fibers containing these putative neurotransmitters are differentially distributed in and around the AVPv in accordance with the cytoarchitectonic organization of this part of the preoptic region. The AVPv itself appears to receive strong inputs from SP-, VAS-, CCK-, and SS-containing pathways, whereas the highest densities of L-ENK-, NT-, 5-HT-, NPY-, and DBH-immunoreactive fibers were found in the cell-sparse zone just lateral to the AVPv. The suprachiasmatic preoptic nucleus (PSCh), a small group of cells located ventral to the AVPv just dorsal to the optic chiasm, contained high densities of alpha-MSH- and ACTH-immunoreactive fibers, as well as substantial numbers of fibers containing catecholamines or NPY. In contrast, a dense plexus of VAS-stained fibers was distributed fairly evenly throughout the AVPv and PSCh. Numerous L-ENK-immunoreactive cell bodies, and moderate numbers of CCK-, NT-, and CRF-stained cell bodies were found in the AVPv. The PSCh contained many TH-stained cells (presumably dopaminergic), in addition to a moderate number of CCK-containing cell bodies, while a high density of NT- and CRF-stained cells were found in the cell-sparse zone lateral to the AVPv, in addition to several CCK-, SP-, VIP-, and TH-containing cells.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:The distribution of neurotransmitter-specific cells and fibers in the anteroventral periventricular nucleus: implications for the control of gonadotropin secretion in the rat. 288 Jun 34

Clinical prospects of an analog of thyrotropin-releasing hormone (DN-1417) and des-tyrosine-gamma-endorphin (DT gamma E) in schizophrenia were examined by using the Brief Psychiatric Rating Scale (BPRS) and the electroencephalogram (EEG). Twelve inpatients with chronic schizophrenia were administered fixed doses of neuroleptics throughout the study. Six patients were treated with DN-1417 (DN-1417 group), and the remaining 6 patients with DT gamma E (DY gamma E group). One mg/day of DN-1417 or DT gamma E was given intramuscularly for 2 consecutive weeks followed by 1 week of no drug treatment. In the DN-1417 group, both total BPRS scores and scores on hallucinatory behaviour and unusual thought content decreased in the first and third weeks. The power values of alpha and beta activities from the frontal area increased in the first and third weeks, whereas an increase in alpha activity and a decrease of high-fast beta activity from the occipital area were obtained during the study. On the other hand, the DT gamma E group failed to show either a decrease in BPRS scores or any remarkable EEG changes except for a slight decrease in beta activity. These results suggest that the positive symptoms of schizophrenia are improved by DN-1417 treatment, and that the alterations in BPRS scores coincide with changes in the frontal EEG.
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PMID:A treatment trial with an analog of thyrotropin-releasing hormone (DN-1417) and des-tyrosine-gamma-endorphin in schizophrenia. 288 64

The effects of pretreatment of rats with an intrahypothalamic injection of 6-hydroxydopamine on the thermal responses induced by intrahypothalamic injection of noradrenaline, prostaglandin E2, thyrotropin-releasing hormone or beta-endorphin were assessed. Administration of either noradrenaline (2-10 micrograms), prostaglandin E2 (10-40 ng), thyrotropin-releasing hormone (0.5-2.0 micrograms) or beta-endorphin (1-3 micrograms) into the preoptic anterior hypothalamus caused a dose-dependent rise in rectal temperature in conscious rats at an ambient temperature of 22 degrees C. In addition, it was found that three intrahypothalamic doses of 10 micrograms of 6-hydroxydopamine at intervals of 2 days caused a significant depletion of noradrenaline in the hypothalamus to 26.4% of control while the concentration of dopamine in the hypothalamus was not significantly reduced at 95.3% of control. Furthermore, the hyperthermic responses induced by prostaglandin E2, thyrotropin-releasing hormone, or beta-endorphin were greatly attenuated after selective depletion of noradrenaline in the hypothalamus in rats. However, selective depletion of noradrenaline did not affect the noradrenaline-induced hyperthermic responses. The data indicate that either prostaglandin E2, thyrotropin-releasing hormone or beta-endorphin may act through the endogenous release of noradrenaline from the hypothalamus to induce hyperthermic responses in rats.
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PMID:Depletion of noradrenaline in the hypothalamus reduces the febrile responses induced by prostaglandin E2, thyrotropin-releasing hormone and beta-endorphin in rats. 293 40


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