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)

This review summarizes the revolutionary impact of brain peptides on our understanding of the nervous system and then discusses the localization, distribution, synthesis, receptor sites, and possible function of 32 brain peptides. The peptides are discussed in three subgroups: I) the opioid peptides, which include beta-endorphin, the enkephalins, and dynorphin; II) the pituitary releasing hormones, most of which are wide-spread in the brain and include corticotropin-releasing hormone, luteinizing hormone-releasing hormone, somatostatin, and thyrotropin-releasing hormone; and III) a selection of 12 other peptides potentially important for neurological function, including vasopressin, oxytocin, substance P, cholecystokinin, bombesin, neurotensin, renin, angiotensin, vasoactive intestinal polypeptide, neuropeptide Y, calcitonin gene-related peptide, and calcitonin. Within each individual peptide section, the possible physiological roles in anterior pituitary hormone release, blood-flow regulation, feeding behavior, temperature regulation, nociception, memory and learning, and movement are reviewed. Further, where noted, the peptide findings in Huntington's, Alzheimer's, Parkinson's and psychiatric diseases are emphasized.
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PMID:Neuropeptides. 187 Jul 24

This study focuses on the involvement of catecholamines and nine different peptides in efferents of the nucleus of the solitary tract to the central nucleus of the amygdala, the bed nucleus of the stria terminalis, and different parabrachial and hypothalamic nuclei in the rat. A double-labeling technique was used that combines a protein-gold complex as the retrograde tracer with immunohistochemistry. Catecholaminergic projection neurons were the most numerous type observed and projected mainly ipsilaterally to all targets studied. Most projections arose from areas overlying the dorsal motor nucleus, mainly the medial nucleus. Neurons synthesizing somatostatin, met-enkephalin-Arg-Gly-Leu, dynorphin B, neuropeptide Y, and neurotensin projected to all structures examined. Somatostatin and enkephalin immunoreactive projection cells were the most numerous. They were located in close proximity to each other, including all subnuclei immediately surrounding the solitary tract, bilaterally. Most dynorphin and neuropeptide Y immunoreactive projection cells were found rostral to that of enkephalinergic and somatostatinergic projections, and mainly in the ipsilateral medial nucleus. Neurotensinergic projections were sparse and from dorsal and dorsolateral nuclei. Substance P and cholecystokinin contribute to parabrachial afferents. The location of substance P immunoreactive projection cells closely resembled that of enkephalinergic and somatostatinergic projections. Projecting cholecystokinin immunoreactive cells were observed in dorsolateral nucleus. Bombesin immunoreactive cells in dorsal nucleus projected to either the parabrachial or hypothalamic nuclei. No vasoactive intestinal polypeptide-containing cells were detected. Thus, most catecholaminergic and neuropeptidergic efferents originated from different populations of cells. It is proposed that catecholaminergic neurons constitute the bulk of solitary efferents and that they may contribute to autonomic neurotransmission. Peptidergic neurons mainly form other subgroups of projections and may play a role in modulating the physiological state of the target nuclei.
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PMID:Neuropeptides and catecholamines in efferent projections of the nuclei of the solitary tract in the rat. 196 68

Neuropeptide Y is found in brain tissue. In dogs it has been shown to enhance activation of the hypothalamic-pituitary-adrenal axis by corticotropin-releasing hormone. It is localized in certain catecholamine neurons and to some extent colocalized with somatostatin. Disturbances of the central noradrenergic system may underlie some forms of alcoholism. Therefore, we compared male alcoholics and normal controls on cerebrospinal fluid (CSF) levels of neuropeptide Y. There was no significant difference between the two groups for neuropeptide Y. There was also no significant difference for CSF levels of growth hormone releasing hormone. However, there were significant positive correlations between CSF levels of neuropeptide Y and CSF levels of corticotropin-releasing hormone, somatostatin, and growth hormone releasing hormone.
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PMID:CSF neuropeptide Y in alcoholics and normal controls. 197 53

Central neurotransmitter and/or neuromodulator candidates reported to affect gastric acid secretion are: (excitatory) acetylcholine, thyrotropin releasing hormone, GABA, oxytocin; (inhibitory) noradrenaline, adenosine, bombesin, calcitonin-gene related peptide, corticotropin releasing factor, beta-endorphin, neurotensin, neuropeptide Y, insulin-like growth factor II and prostaglandins. Regulation of gastric acid secretion by central administration of these substances in experimental animals such as rats and dogs are briefly reviewed, and central inhibitory mechanisms of this function are discussed based on our studies with noradrenaline and bombesin. Roles of hypothalamic nuclei such as the ventromedial nucleus and the lateral hypothalamus in regulation of autonomic nerve activities are also described as an introductory note.
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PMID:[Central neurotransmitters and regulation of gastric acid secretion]. 198 Jun 59

This paper examines the treatment of obesity, using a feedback model of nutrient regulation. A feedback model contains afferent signals and a central controller that transduces afferent information into efferent signals that modulate the controlled system. Using this model and the receptor hypothesis for drug action, a variety of current and potential therapeutic approaches are discussed. Among the more promising approaches would be cholecystokinin agonists, small molecules that mimic ketoacids, agonists to corticotropin-releasing hormone, beta-3 agonists, antagonists to opioid peptides, antagonists to neuropeptide Y, glucocorticoid receptor antagonists, and growth hormone agonists. Since a number of mechanisms can influence body fat and nutrient partitioning, it is likely that optimal therapy will involve use of more than one pharmacologic agent.
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PMID:Treatment for obesity: a nutrient balance/nutrient partition approach. 201 19

The objectives of these studies were to examine the release of gonadotropin-releasing hormone (GnRH) and beta-endorphin-like activity (beta-EP) from macaque hypothalami, and the release of luteinizing hormone (LH) and GnRH-induced LH from macaque anterior pituitaries in response to neuropeptide Y (NPY) treatment. Anterior hypothalamic (AH) and mediobasal hypothalamic (MBH) blocks of tissues and the adenohypophysis were bisected along the midline into two equal-sized fragments. Fragments were superfused with medium for 3 h, followed by 3 h of either NPY (80 nM) or medium alone. In a separate experiment, adenohypophyseal (AP) fragments were superfused in accordance with the same protocol (3 h medium - 3 h NPY or medium) except that exogenous GnRH (352 nM) was added for 30 min at the beginning of hour 3 and again at the beginning of hour 6. Immunoactive GnRH, beta-EP, and LH levels were measured in superfusate samples (400 microliters) collected at 10-min intervals. GnRH levels rose within 20-30 min of initiation of NPY treatment, and elevated GnRH release was sustained for the duration of NPY exposure of both AH and MBH fragments from ovarian intact (INT) rhesus (Macaca mulatta: n = 8; p less than 0.05) or Japanese (Macaca fascicularis; n = 4; p less than 0.01) macaques. NPY treatment had no effect on either AH or MBH fragments isolated from ovariectomized (OVX) rhesus macaques (n = 4 for AH, and n = 5 for MBH). In AP fragments isolated from INT rhesus macaques (n = 8), NPY stimulated LH release within 1 h of treatment (p less than 0.05), whereas NPY had no effect on pituitaries from OVX animals (n = 4).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effects of neuropeptide Y on the in vitro release of gonadotropin-releasing hormone, luteinizing hormone, and beta-endorphin and pituitary responsiveness to gonadotropin-releasing hormone in female macaques. 204 72

Previous studies have shown that the release of melanotropin from frog neurointermediate lobes is under the control of two neuropeptides: thyrotropin-releasing hormone (TRH) stimulates, while neuropeptide Y (NPY) inhibits alpha-melanocyte-stimulating hormone (alpha-MSH) secretion from intact neurointermediate lobes in vitro. The aim of the present study was to investigate possible interactions between the two regulatory peptides at the pituitary level. Whole neurointermediate lobes or acutely dispersed pars intermedia cells from Rana ridibunda were perifused in vitro for 2 to 7.5 hr and the concentrations of alpha-MSH released into the effluent perifusate were monitored by radioimmunoassay. Administration of TRH (10(-7) M) or NPY (10(-7) M) to dispersed cells induced, respectively, marked stimulation or inhibition of alpha-MSH release. The effects of the two neuropeptides were similar to those observed using intact neurointermediate lobes, suggesting that TRH and NPY act directly on melanotropic cells. Perifused whole neurointermediate lobes were exposed to NPY (10(-8) to 3 x 10(-7) M) for 120 min and a single dose of TRH (10(-8) M) was administered during the prolonged infusion of NPY. Using this procedure, we observed a dose-dependent inhibition of TRH-evoked alpha-MSH release. These data support the concept that TRH and NPY act through a common intracellular pathway to regulate alpha-MSH release.
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PMID:Neuropeptide Y inhibits thyrotropin-releasing hormone-induced stimulation of melanotropin release from the intermediate lobe of the frog pituitary. 210 15

A fairly high number of neuropeptide Y (NPY) and adrenocorticotropic hormone (ACTH) immunoreactive (ir) neuronal perikarya and dense networks of NPY-ir fibers are present in the hypothalamic arcuate nucleus of rats. Light and electron microscopic double immunolabeling techniques were used to demonstrate morphological connections between NPY-ir nerve fibers and ACTH-ir neurons here. Silver-gold intensified diaminobenzidine (DAB) labeling of perikaryal-dendritic immunoreactivity followed by a second, non-intensified DAB chromogen labeling of immunoreactive nerve terminals was used and recommended in the above sequence as a method of choice for the detection of synaptic contacts with double-labeling technique. By this way, NPY-immunoreactivity was localized in axons and axonal terminals forming a variety of conventional synaptic contacts with ACTH-ir neuronal perikarya and dendrites in the arcuate nucleus.
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PMID:Neuropeptide Y innervation of ACTH-immunoreactive neurons in the arcuate nucleus of rats: a correlated light and electron microscopic double immunolabeling study. 215 82

An immunoneutralization technique with specific antibodies was used to explore the role of endogenous neuropeptide Y (NPY) in the adrenocorticotropic hormone (ACTH) release after hypoglycemic stress in the dog. Dogs received injections of rabbit antihuman NPY gamma-globulin (anti-NPY) or normal gamma-globulin (NGG) into the third cerebral ventricle, which was followed by i.v. injection of insulin. Hypoglycemia of a 40% fall in systemic glucose levels occurred in anti-NPY-treated dogs as well as NGG-treated animals. An intraventricular administration of anti-NPY significantly inhibited the ACTH and cortisol release to hypoglycemia, but had no effect on the pancreatic polypeptide (PP) response. These findings suggest involvement by endogenous NPY in the ACTH secretion induced by hypoglycemia.
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PMID:Brain neuropeptide Y in the control of adrenocorticotropic hormone secretion in the dog. 215 50

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


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