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 effect of acute central administration of Neuropeptide Y (NPY) to adult male rats on the brain content of corticotropin-releasing factor immunoreactivity (CRF-ir) was investigated. The brain regions studied included frontal cortex, hippocampus, medulla-pons, midbrain-thalamus, cerebellum, neurointermediate lobe of pituitary, median eminence and the remaining hypothalamus. CRF-ir was determined in each of these regions using a radioimmunoassay specific for rat CRF. CRF-ir was found to be significantly increased in the major site of CRF localization in the brain, the hypothalamus, in NPY-treated rats as compared to vehicle-treated controls either 15 minutes (p less than 0.025) or 45 minutes (p less than 0.005) post-injection. This increase was localized to the median eminence (p less than 0.05 after 15 minutes, p less than 0.01 after 45 minutes). No statistically significant differences were noted in any of the other brain regions assessed. Plasma adrenocorticotropin levels were also found to increase following NPY treatment, an effect which became significant after 45 minutes (p less than 0.05). These data show that NPY can alter the content of hypothalamic CRF and may play a role in its regulation.
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PMID:Neuropeptide Y administration acutely increases hypothalamic corticotropin-releasing factor immunoreactivity: lack of effect in other rat brain regions. 282 49

Neuropeptide Y in concentrations from 10(-8) to 10(-6) M inhibits the release of alpha-MSH from the frog (Rana pipiens) pituitary in a reversible, sustained, and concentration-related manner. However, it does not inhibit the release of alpha-MSH from the rat pars intermedia. Thus, while neuropeptide Y may play a role in the control of alpha-MSH release in amphibia, it appears not to be a regulatory peptide for the mammalian pars intermedia.
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PMID:Neuropeptide Y does not inhibit the release of alpha-MSH from the pars intermedia of the rat adenohypophysis. 284 69

Following intraventricular (i.v.t.) administration of increasing doses of neuropeptide Y (NPY; 7.5-750 pmol/rat) the catecholamine levels and turnover were quantitatively measured in discrete hypothalamic regions by means of histofluorometry. In the same rats the adenohypophyseal hormones as well as vasopressin, aldosterone (ALDO) and corticosterone (CORTICO) levels in serum were determined. Neuropeptide Y seems to induce a biphasic change in amine utilization in the tuberoinfundibular dopamine (DA) neurons and in the noradrenergic (NA) utilization in various hypothalamic areas. Thus, the lowest doses seem to inhibit the catecholamine utilization while higher doses seem to enhance it. NPY (250-750 pmol) reduced the serum levels of thyreotropine (TSH), prolactin (PRL) and growth hormone (GH) but increased CORTICO, adrenocorticotropin (ACTH) and ALDO serum levels. In conclusion, it is suggested that the NPY induced changes in DA utilization in the tuberoinfundibular DA neurons may contribute to the NPY induced changes in PRL and TSH secretion. The increases in paraventricular NA utilization may contribute to the increases in ACTH, ALDO and CORTICO secretion induced by NPY. These data give further support for NPY as an important neuroendocrine modulator.
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PMID:Further studies on the effects of central administration of neuropeptide Y on neuroendocrine function in the male rat: relationship to hypothalamic catecholamines. 358 2

The presence of neuropeptide tyrosine (NPY) in the intermediate lobe of the frog pituitary was demonstrated using indirect immunofluorescence, the immunogold technique and a specific radioimmunoassay combined with high pressure liquid chromatography (HPLC). A high density of NPY-containing fibers, was found among the parenchymal cells of the intermediate lobe. These fibers originated from the ventral infundibular nucleus, travelled via the median eminence to the pars intermedia. At the electron microscopic level, NPY-like material was found exclusively in nerve fibers where the product of the immunoreaction was associated to dense-core vesicles. High concentrations of NPY-like peptide were found in neurointermediate lobe extracts. After Sephadex G-50 gel filtration the major peak of immunoreactive material appeared to co-elute with synthetic porcine NPY. Conversely, HPLC analysis revealed that the NPY-like peptide of the frog pituitary had a retention time shorter than the porcine NPY. The localization of NPY-like material in the pars intermedia suggested a possible role of NPY in the regulation of melanotropic cell secretion. In fact, graded concentrations of synthetic NPY induced a dose-dependent inhibition of alpha-melanotropin (alpha-MSH) release in vitro. The lack of effect of a dopaminergic antagonist on NPY-induced alpha-MSH release inhibition demonstrated that the local dopaminergic system could not account for the NPY action. These results indicate that NPY located in the hypothalamo-hypophyseal system of the frog may act as a melanotropin-release inhibiting factor.
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PMID:Neuropeptide Y in the intermediate lobe of the frog pituitary acts as an alpha-MSH-release inhibiting factor. 375 90

Neurotensin (NT), administered intracisternally to mice, produced significant dose-dependent antinociception in three analgesic tests: tail immersion, hot-plate and acetic acid writhing. Naloxone (1-5 mg/kg), an opiate antagonist administered i.p. 20 min before NT administration, did not significantly alter NT-induced antinociception in any of these tests; naloxone did significantly reverse beta-endorphin-induced antinociception. However, centrally and peripherally administered thyrotropin-releasing hormone antagonized NT-induced (but not beta-endorphin-induced) antinociception. Equimolar doses of another tripeptide (Pro-Leu-Gly-NH2; melanostatin) did not alter the effects of NT. The data obtained in this study confirm NT-induced antinociception, provide further evidence that NT does not activate naloxone-sensitive opiate receptors and demonstrate that this brain effect of NT is antagonized by thyrotropin-releasing hormone. These findings therefore support the hypothesis that NT and thyrotropin-releasing hormone are functional antagonists in the central nervous system.
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PMID:Neurotensin-induced antinociception in mice: antagonism by thyrotropin-releasing hormone. 611 61

Neuropeptide Y (NPY), a major brain neurotransmitter, is expressed in neurons of the hypothalamic arcuate nucleus (ARC) that project mainly to the paraventricular nucleus (PVN), an important site of NPY release. NPY synthesis in the ARC is thought to be regulated by several factors, notably insulin, which may exert an inhibitory action. The effects of NPY injected into the PVN and other sites include hyperphagia, reduced energy expenditure and enhanced weight gain, insulin secretion, and stimulation of corticotropin and corticosterone release. The ARC-PVN projection appears to be overactive in insulin-deficient diabetic rats, and could contribute to the compensatory hyperphagia and reduced energy expenditure, and pituitary dysfunction found in these animals; overactivity of these NPY neurons may be due to reduction of insulin's normal inhibitory effect. The ARC-PVN projection is also stimulated in rat models of obesity +/- non-insulin diabetes, possibly because the hypothalamus is resistant to inhibition by insulin; in these animals, enhanced activity of ARC NPY neurons could cause hyperphagia, reduced energy expenditure, and obesity, and perhaps contribute to hyperinsulinemia and altered pituitary secretion. Overall, these findings suggest that NPY released in the hypothalamuss, especially from the ARC-PVN projection, plays a key role in the hypothalamic regulation of energy balance and metabolism. NPY is also found in the human hypothalamus. Its roles (if any) in human homeostasis and glucoregulation remain enigmatic, but the animal studies have identified it as a potential target for new drugs to treat obesity and perhaps NIDDM.
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PMID:Neuropeptide Y, the hypothalamus, and diabetes: insights into the central control of metabolism. 747 13

We studied interleukin-1 beta (IL-1 beta), beta 2-microglobulin (beta 2-m), beta-endorphin, substance P, neuropeptide Y and somatostatin concentrations in the cerebrospinal fluid of 13 patients with dementia of the Alzheimer type (DAT), 13 patients with multi-infarct dementia (MID) and 15 age-matched control subjects. Substance P was significantly lower in DAT than in controls (P < 0.05), as well as somatostatin in DAT as compared to both controls (P < 0.01) and MID (P < 0.05), whereas beta 2-m was higher in DAT than in controls (P < 0.01). Neuropeptide Y, beta-endorphin and IL-1 beta showed similar concentrations in the three groups studied. A significantly positive correlation was observed between IL-1 beta and substance P (r = 0.79, P < 0.01) and somatostatin (r = 0.75, P < 0.05) in DAT, which was not observed in MID. In addition, beta 2-m showed a negative correlation with IL-1 beta (r = -0.73, P < 0.05) in DAT, and age correlated negatively with IL-1 beta in controls and MID, but positively in DAT. Therefore, these results support the idea that an altered relationship may exist in Alzheimer's disease between the nervous and immune system.
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PMID:Relationship of interleukin-1 beta and beta 2-microglobulin with neuropeptides in cerebrospinal fluid of patients with dementia of the Alzheimer type. 769 56

Neuropeptidergic innervation of the human prostate, seminal vesicle and vas deferens was investigated by immunohistochemical methods. The innervation pattern of all organs was very dense. Neuropeptide Y- and tyrosine hydroxylase-positive nerve fibers were most abundant and localized mainly in the smooth muscle layer. On the contrary, vasoactive intestinal polypeptide-positive nerve fibers were mainly found beneath the epithelium. Also leu-enkephaline-, peptide histidine isoleusine- and calcitonin gene-related peptide-positive nerve fibers could be observed in all organs, but somatostatin-positive nerves only in the prostate and seminal vesicle and met-enkephalin- and substance P-positive nerves only in the prostate.
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PMID:Peptidergic innervation of the human prostate, seminal vesicle and vas deferens. 777 Nov 81

1. Melanostatin, a thirty-six amino acid peptide recently isolated from the frog brain due to its ability to inhibit alpha-melanocyte-stimulating hormone (alpha-MSH) release, is the amphibian counterpart of mammalian neuropeptide Y (NPY). The effect of synthetic melanostatin on the bioelectrical activity of cultured frog melanotrophs was studied in 124 cells by using the whole-cell patch-clamp technique. 2. In current-clamp experiments, melanostatin (1 microM) provoked a reversible hyperpolarization and a suppression of spontaneous action potentials. In some cells the hyperpolarizing response was absent, but an arrest of spike firing still occurred. 3. Melanostatin-induced hyperpolarization was associated with a decrease in membrane resistance. In voltage-clamp experiments, melanostatin induced an outward current at a constant command potential. This hyperpolarizing outward current appeared to be carried by potassium ions. 4. Cell dialysis with the non-hydrolysable GTP analogue guanosine-5'-O-(3-thiotriphosphate) (GTP gamma S) sustained the outward current produced by melanostatin. Dopamine (1 microM), which generates a similar hyperpolarizing outward current in frog melanotrophs, was not capable of increasing the current provoked by melanostatin and sustained by GTP gamma S. 5. Melanostatin also modulated voltage-operated currents. The amplitude of voltage-activated potassium current was increased by 30%. 6. Melanostatin reduced the fast sodium current. This inhibitory effect was rather persistent compared to the other modulated currents. 7. Melanostatin markedly scaled down high voltage-activated N- and L-like calcium currents. The activation kinetics of these two calcium currents were not altered by the peptide. 8. Pretreatment of melanotrophs with pertussis toxin (1 microgram ml-1) blocked melanostatin-induced inhibition of N- and L-like calcium currents. 9. It is concluded that the NPY-related peptide melanostatin generates a very complex pattern of electrical responses in frog melanotrophs, including hyperpolarization and modulation of voltage-activated currents underlying action potentials. G proteins appear to mediate at least part of these effects.
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PMID:Melanostatin (NPY) inhibited electrical activity in frog melanotrophs through modulation of K+, Na+ and Ca2+ currents. 791 31

Neuropeptide Y (NPY) has a stimulatory effect on adrenocorticotropin (ACTH) and corticotropin-releasing factor (CRF) release. In the present study, to investigate the effect of NPY on CRF synthesis, the effect of centrally administered NPY on CRF messenger RNA (mRNA) levels in rat hypothalamus was examined under pentobarbital anesthesia. The administration of 0.01, 0.1 and 1 nmol of NPY into the lateral ventricle dose-dependently Increased the plasma ACTH levels, as well as the levels of proopiomelanocortin mRNA in the anterior pituitary. The CRF mRNA level in the hypothalamus also increased after administration of 0.1 and 1 nmol of NPY in a dose-dependent manner. The administration of 3 nmol of phentolamine or propranolol failed to block 0.1 nmol NPY-induced ACTH release or 1 nmol NPY-stimulated CRF mRNA levels in the hypothalamus. These results Indicate that the central administration of NPY increases the CRF mRNA levels in the hypothalamus and the probable CRF release, which increases the proopiomelanocortin mRNA levels and ACTH secretion in the anterior pituitary. Therefore, NPY seems to play a physiological role in the regulation of the release and synthesis of CRF in the hypothalamus.
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PMID:Neuropeptide Y increases the corticotropin-releasing factor messenger ribonucleic acid level in the rat hypothalamus. 839 33


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