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)

There is increasing evidence that neuropeptide Y (NPY) affects the release of pituitary hormones, including adrenocorticotropic hormone (ACTH). The present study was designed to clarify the mechanism by which NPY activates the hypothalamic-pituitary-adrenal (HPA) axis in the dog. Mongrel dogs were equipped with a chronic cannula allowing intra-third (i.t.v.) or intra-lateral (i.l.v.) cerebroventricular administration. A 1.19 nmol, i.t.v. dose of NPY produced as great an ACTH and cortisol response as did equimolar ovine corticotropin releasing factor (CRF). This action of NPY was dose-dependent and shared by peptide YY (PYY) and pancreatic polypeptide (PP), other members of the PP family peptide. Intravenously (i.v.) administered NPY (1.19-11.9 nmol) was much less potent than i.v. CRF in stimulating ACTH and cortisol secretion. However, i.v. NPY significantly increased plasma ACTH and cortisol concentrations, raising the possibility that NPY may modulate the activity of corticotrophs. We next investigated the possible relationship between NPY and CRF on the HPA axis. Pretreatment with a novel CRF antagonist, alpha-helical CRF9-41 (130.9 nmol i.t.v. or 261.5 nmol i.v.), partly but significantly attenuated the ACTH and cortisol responses to i.t.v. NPY (1.19 nmol). Furthermore, adding a subthreshold dose of i.t.v. NPY (0.119 nmol) to i.t.v. CRF (1.19 nmol) or i.v. NPY (2.38 nmol) to i.v. CRF (0.595 nmol) resulted in the potentiation of CRF-induced ACTH secretion. These results indicate that NPY may activate the HPA axis in concert with CRF probably at hypothalamic and/or pituitary levels. The present findings that NPY evokes ACTH secretion and potentiates the effectiveness of CRF as a secretagogue, together with high concentrations of NPY in the hypothalamus and pituitary portal blood, suggest the NPY is involved in the multihormonal control of ACTH release.
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PMID:[The effect of neuropeptide Y on the hypothalamic-pituitary-adrenal axis in the dog]. 216 47

There is increasing evidence that neuropeptide Y (NPY) affects the release of pituitary hormones, including adrenocorticotropic hormone (ACTH). The present study was designed to clarify the mechanism by which NPY activates the hypothalamic-pituitary-adrenal (HPA) axis in the dog. Mongrel dogs were equipped with a chronic cannula allowing intra-third (i.t.v.) or intra-lateral (i.l.v.) cerebroventricular administration. A 1.19 nmol, i.t.v. dose of NPY produced as great an ACTH and cortisol response as did equimolar ovine corticotropin releasing factor (CRF). This action of NPY was dose-dependent and shared by peptide YY (PYY) and pancreatic polypeptide (PP), other members of the PP family peptide. Intravenously (i.v.) administered NPY (1.19-11.9 nmol) was much less potent than i.v. CRF in stimulating ACTH and cortisol secretion. However, i.v. NPY significantly increased plasma ACTH and cortisol concentrations, raising the possibility that NPY may modulate the activity of corticotrophs. We have next investigated the possible relationship between NPY and CRF on the HPA axis. Pretreatment with a novel CRF antagonist, alpha-helical CRF9-41 (130.9 nmol i.t.v. or 261.8 nmol i.v.), partly but significantly attenuated the ACTH and cortisol responses to i.t.v. NPY (1.19 nmol). Furthermore, adding a subthreshold dose of i.t.v. NPY (0.119 nmol) to i.t.v. CRF (1.19 nmol) or i.v. NPY (2.38 nmol) to i.v. CRF (0.595 nmol) resulted in the potentiation of CRF-induced ACTH secretion. These results indicate that NPY may activate the HPA axis in concert with CRF probably at hypothalamic and/or pituitary levels. The present findings that NPY evokes ACTH secretion and potentiates the effectiveness of CRF as a secretagogue, together with high concentrations of NPY in the hypothalamus and pituitary portal blood, suggest that NPY is involved in the multihormonal control of ACTH release.
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PMID:Effect of neuropeptide Y on the hypothalamic-pituitary-adrenal axis in the dog. 253 98

This study examined the number of met-enkephalin, dynorphin A 1-8, and neurotensin immunoreactive (IR) neurons in the marginal zone (lamina I) at one thoracic (T8:cat,T9:rat), one midlumbar (L5:cat,L4:rat), and one lower lumbar or sacral (S1:cat,L6:rat) spinal cord segment in the cat and rat. Marginal zone IR neurons ranged 10-70 microns in diameter in cats and 10-50 microns in rats and were flattened, pyramidal, fusiform, or polygonal in morphology. Immunoreactive neurons for each peptide in both species were found in the marginal zone at all spinal levels, but with a differential segmental distribution. The average number of IR neurons per 50-microns section generally was lowest in thoracic cord and greatest in lower lumbar/sacral cord for all peptides. For enkephalin and dynorphin, the estimated total number of IR neurons per segment and number of IR neurons per volume (mm3) generally were lowest in the midlumbar segments and highest in the thoracic and lower lumbar/sacral cord. For neurotensin, the estimated total number of neurons per segment remained lowest in the thoracic and largest in the lower lumbar/sacral cord. The number of neurotensin IR neurons per volume was equal in the thoracic and midlumbar cord, but remained highest at lower lumbar/sacral levels. The IR neurons quantified in this study may be interneurons or may serve as supraspinal projection neurons. The large number of IR neurons observed in segments receiving a relatively large visceral afferent input suggests that some of these neurons may be involved in visceral sensory processing. In addition, the segmental distribution of the IR neurons indicates that physiological and pharmacological studies on the effects of opioid and/or neurotensin peptides should be interpreted in light of the spinal segment(s) investigated.
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PMID:Comparison of met-enkephalin, dynorphin A, and neurotensin immunoreactive neurons in the cat and rat spinal cords: II. Segmental differences in the marginal zone. 256 38

A large portion of the human pro-opiomelanocortin (POMC) peptide corresponding to amino acid residues 59-241 has been cloned and expressed in Escherichia coli. A 1.0 kb DNA fragment encoding this peptide was cloned into the expression vectors pUC8 and pUR291. Plasmid pJMBG51 (a pUC8 recombinant) was found to direct the expression of a 24 kDa peptide. The recombinant pUR291 (pJMBG52) was shown to produce a beta-galactosidase fusion protein of 140 kDa. Western blot analysis showed that both the 24 kDa and 140 kDa peptides are recognized by antibodies raised against POMC-derived peptides. The beta-galactosidase fusion protein has been partially purified from crude E. coli cell lysates using affinity chromatography on p-amino-benzyl-1-thio-beta-D-galactopyranoside agarose.
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PMID:Expression and partial purification of human pro-opiomelanocortin in Escherichia coli. 267 85

This study compared the distribution of methionine enkephalin-, dynorphin A 1-8-, and neurotensin-immunoreactive (IR) perikarya in laminae I and IV-VII of selected segments of lumbar spinal cord of cat(L5) and rat(4). Immunoreactive neurons for each peptide were found throughout the dorsal horn and dorsal lamina VII but were quantified only within laminae I and IV-VII. In lamina I, both large (greater than 20 micron) and small (less than 20 micron) IR neurons were identified. Large IR neurons for each peptide in both species resembled Waldeyer neurons studied by Golgi stain and were outnumbered by small IR neurons. Comparison among the laminae of the distribution of met-enkephalin IR neurons showed a similar pattern in the two species with the majority of IR neurons (greater than 65%) in laminae V and VI. Differences in laminar distribution occurred between species for the other peptides. Dynorphin IR neurons were greatest in number in lamina V in rat but greatest in number in laminae I and V in cat. Neurotensin IR neurons occurred predominantly in cat lamina I but were nearly equal in density in rat laminae I and VI. The topographic distribution of each peptide in laminae V and VI was similar between the two species with IR neurons occurring laterally in lamina V and more medially in lamina VI. Comparisons between species of the numbers of IR neurons/segment indicated distinct relationships for each peptide. The number of met-enkephalin IR neurons in laminae of cat L5 was generally two times greater than the number of IR neurons in the same laminae of rat L4, except in laminae I and IV, where the numbers were nearly equal. In contrast, the number of dynorphin IR neurons in cat laminae was generally one-half the number in rat, except in lamina I, where the number in cat was two times greater than rat. A high degree of variability occurred in laminar comparisons of neurotensin IR neurons. Neurotensin IR neurons in lamina I of cat outnumbered those of rat 2:1, but in laminae IV-VII, the ratio of cat to rat IR neurons varied from 1:1 to 1:20. The met-enkephalin, dynorphin, and neurotensin IR neurons quantified in this study may be interneurons or may serve as projection neurons to brainstem and/or thalamic nuclei. The observed differences in distribution may be relevant to differences in spinal cord physiology in the two species.
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PMID:Comparison of met-enkephalin-, dynorphin A-, and neurotensin-immunoreactive neurons in the cat and rat spinal cords: I. Lumbar cord. 288 Aug 79

The addition of orally administered bromocriptine mesylate to cyproheptadine hydrochloride therapy completely normalized urinary-free cortisol levels for three months in a 21-year-old woman with Cushing's syndrome in whom results from standard dexamethasone suppression and metyrapone stimulation tests as well as baseline corticotropin levels were originally compatible with a diagnosis of an occult pituitary adenoma. When transsphenoidal exploration of the sella turcica was unsuccessful and hypercortisolism persisted, the source of corticotropin was discovered using petrosal sinus and venal caval catheterization. A 1 X 1.5-cm carcinoid tumor of the lung was identified and removed, thereby correcting the hypercortisolism. The tumor was demonstrated by immunoperoxidase staining to contain corticotropin. Orally administered bromocriptine, with or without cyproheptadine therapy, may be useful in the palliative treatment of some patients with carcinoid or other ectopic corticotropin-producing tumors. We postulate that bromocriptine therapy acted directly on carcinoid tumor cells to directly inhibit corticotropin production by a dopaminergic mechanism.
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PMID:Prolonged suppression of a corticotropin-producing bronchial carcinoid by oral bromocriptine. 303 81

Gadolinium diethylenetriamine pentaacetic acid (DTPA) enhanced magnetic resonance imaging was performed in eight patients with Cushing disease and surgically proven pituitary microadenomas. A 1.5 T scanner was used with 3 mm contiguous slices. Short repetition times (TR), short echo times (TE), and long TR, long TE sequences were obtained before and serially after intravenous administration of Gd-DTPA. Three of eight (38%) microadenomas were undetectable both without and with Gd-DTPA: one post-Gd-DTPA scan was false positive on the side opposite the adenoma. Hemihypophysectomy based on a petrosal sinus adrenocorticotropic hormone (ACTH) gradient cured all three patients. Two microadenomas (25%) were visible as hypointense foci following Gd-DTPA but not on unenhanced scans. The remaining three microadenomas (38%) were seen before and after Gd-DTPA on T1-weighted images. In this small series of ACTH-producing microadenomas, one-third were seen on unenhanced 1.5 T scans, one-third were seen only after Gd-DTPA, and one-third were not imaged even with Gd-DTPA enhancement.
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PMID:Gadolinium DTPA enhanced MR imaging of ACTH-secreting microadenomas of the pituitary gland. 317 Aug 30

These studies were designed to further test the hypothesis that corticotropin-releasing hormone (CRH) is released from axons innervating the noradrenergic neurons of the locus coeruleus (LC) and serves to activate these neurons during stress responses. Specifically, the effects of exogenous CRH on the electrophysiological activity of LC neurons in unanesthetized rats were characterized. Intracerebroventricular (I.C.V.) injection of CRH (0.3-3.0 micrograms) caused a dose-dependent increase in LC spontaneous discharge rates that became statistically significant 6-9 min after injection and was still evident 30-40 min later. A 1.0 and 3.0 micrograms amount of CRH caused peak increases of 86 +/- 32% and 184 +/- 29% (SEM), respectively. In contrast, neither the lowest dose of CRH (0.3 microgram) nor a high dose of Ala 14CRH (3.0 micrograms), an inactive analog of CRH, altered LC spontaneous activity. The effects of CRH administration on sensory-evoked activity of LC neurons were also determined. As previously reported (Foote et al., 1980; Aston-Jones and Bloom, 1981b), the repeated presentation of auditory tone stimuli resulted in a brief enhancement of LC discharge, which was usually followed by a period of relatively decreased activity. Administration of 1.0 or 3.0 micrograms CRH enhanced basal discharge during sensory testing, but discharge rates during the excitatory component of the sensory response were not altered. Quantitative analyses revealed that these doses of CRH produced a statistically significant decrease in the ratio of sensory-evoked to basal discharge rates. Additional analyses of the temporal distribution of discharge activity for individual recording sites during sensory testing demonstrated that 1.0 and 3.0 micrograms CRH altered relative response magnitudes to a statistically significant extent in 7 of 10 and 5 of 7 cases, respectively, while 0.3 microgram CRH and 3.0 micrograms Ala 14CRH were without effect. The present results are consistent with previous studies of CRH effects on LC activity in anesthetized rats (Valentino et al., 1983; Valentino and Foote, 1987). However, in unanesthetized animals, CRH is more potent in increasing tonic activity and does not decrease the absolute magnitude of sensory-evoked activity. The present results support the hypothesis that CRH released from fibers innervating the LC may affect the tonic activity of these cells and the relationship between tonic discharge and phasic, sensory-evoked activity.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Corticotropin-releasing hormone increases tonic but not sensory-evoked activity of noradrenergic locus coeruleus neurons in unanesthetized rats. 325 21

Five opioid peptides (immunoreactivity) derived from their respective opioid precursors were measured in neuroblastoma-glioma hybrid cells (NG 108CC15; pmol/g protein): heptapeptide (Tyr-Gly-Gly-Phe-Met-Arg-Phe), 13.0 +/- 2.6; alpha-neoendorphin, 6.6 +/- 0.8; dynorphin A, 4.4 +/- 1.5; dynorphin A 1-8, 1.3 +/- 0.29; beta-endorphin, 0.3 +/- 0.13. These peptides originate from preproenkephalin A (heptapeptide), prodynorphin (alpha-neonedorphin, dynorphin A, dynorphin A 1-8) and proopiomelanocortin (beta-endorphin). The data suggest the expression of all three known opioid precursors in a single hybrid cell line, permitting a simultaneous investigation of the processing of different opioid peptides under identical experimental conditions.
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PMID:Evidence for the expression of peptides derived from three opioid precursors in NG 108CC15 hybrid cells. 356 21

Central administration of a Corticotropin-Releasing Factor (CRF) antagonist is well documented to attenuate a variety of behavioral responses to several distinct stressors; however, it is not yet clear whether the activation of CRF neurons is dependent on the type or intensity of the experimental stressor, or rather on the particular behavioral response to stress under study. To test the generality of the stress-protective effect of the CRF antagonist, alpha-helical CRF9-41, (1, 5 or 25 micrograms intracerebroventricularly), the present experiments employed a sensitive index of anxiogenic-like behavior by measuring suppression in exploration on the elevated plus-maze following exposure to social, swim, or restraint stressors. A 1 but not 5 or 25 micrograms dose of the CRF antagonist administered just prior to social, swim, or restraint stress reversed the stress-induced inhibition of exploratory behavior. Chlordiazepoxide and the steroid anesthetic, alphaxalone, also attenuated the anxiogenic-like effect of restraint stress and elevated the baseline exploratory behavior of nonstressed control groups. Although the stressors produced a graded secretion of adrenocorticotropin (ACTH) with the ranking restraint > swim > social, the relative amplitude of behavioral reactivity to social, swim, and restraint stress was comparable. The relative efficacy of the CRF antagonist to reverse the stressor effects was also comparable. These results suggest that antagonism of activated brain CRF systems attenuates the behavioral response to stress regardless of the type or intensity of the stressor as measured by ACTH secretion.
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PMID:Anti-stress action of a corticotropin-releasing factor antagonist on behavioral reactivity to stressors of varying type and intensity. 786 99


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