UNIPROT:P20366 - FACTA Search

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Query: UNIPROT:P20366 (substance P)
21,176 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Substance P-like immunoreactivity was assayed in superfusates of guinea-pig ureters following stimulation of afferent fibres with capsaicin, potassium chloride and the calcium channel agonist Bay K 8644. Capsaicin-evoked release of substance P-like immunoreactivity was calcium-dependent but unaffected by cobalt. Under appropriate conditions release was dose-related (ED50 = 610 nM) and reproducible. Selective desensitization to capsaicin could be demonstrated following prolonged exposure to different doses of capsaicin. No desensitization to capsaicin was observed following afferent fibre stimulation with a combination of Bay K 8644 and K+, which released a similar amount of substance P-like immunoreactivity as a desensitizing capsaicin stimulus. These data suggest that depletion of releasable substance P-like reactivity is unlikely to account for selective desensitization of ureteric primary afferent fibres to capsaicin.
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PMID:Desensitization and capsaicin-induced release of substance P-like immunoreactivity from guinea-pig ureter in vitro. 247 71

Intracellular recordings were made from neurons (n = 121) in the inferior mesenteric ganglion (IMG) in guinea-pig. The afterspike hyperpolarization (ASH) following a single action potential was studied in IMG cells which received an excitatory, cholinergic innervation from mechanosensory nerves in the gastrointestinal tract. The amplitude of ASH was dependent on the membrane potential of IMG cells and the concentration of K+ in the bathing solution. The reversal potential of ASH (-80- -90 mV, in normal Krebs solution) appeared to follow the equilibrium potential for K+, as [K+]o was changed, suggesting that ASH was the product of K+-efflux. Further evidence suggested that a major component of the K+-efflux was dependent on the concentration of Ca2+ in the bathing medium. Elevation and reduction of [Ca2+]o increased and decreased, respectively, the amplitude and duration of ASH. In the presence of tetrodotoxin, depolarizing current pulses elicited spike-like events which (1) were dependent on [Ca2+]o and the degree of depolarization by current-clamp and (2) were followed by afterhyperpolarizations that were also dependent on [Ca2+]o and degree of depolarization by current-clamp. In the combined presence of tetrodotoxin and tetraethylammonium, depolarizing current pulses elicited prolonged action potentials (up to 100 ms in duration) followed by prolonged ASH (up to 3 s in duration). Spike-like events, prolonged action potentials and their afterhyperpolarizations were reduced in amplitude and duration when the calcium-channel blocking ion, Co2+, or blocking drug, verapamil, was present in the bathing medium. In normal Krebs solution, the ASH of action potentials produced by nerve stimulation was reduced but not abolished in the presence of Co2+. These results suggested that Ca2+ entered IMG cells during depolarization and activated the K+-conductance mechanisms responsible for the ASH. However, an initial component of the ASH may have involved other voltage-dependent K+-currents known to be activated during the excitation of sympathetic neurons. The amplitude and duration of ASH differed during non-synaptic and synaptic excitation of IMG cells, and differed when action potentials resulted from fast and slow EPSPs. In addition, the amplitude and duration of ASH were altered by noradrenaline, by the cholinomimetic, carbachol, and by 3 neuropeptides present in the IMG, namely leucine-enkephalin, substance P and vasoactive intestinal polypeptide.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Afterspike-hyperpolarization of neurons in the inferior mesenteric ganglion in guinea-pig. 290 79

AtT20/D16v is a clonal strain of mouse pituitary tumor cells which synthesizes and secretes ACTH. Somatostatin, a hypothalamic tetradecapeptide, has been shown to inhibit the release of PRL, GH, and TSH from the pituitary gland. We have characterized specific binding sites for somatostatin on AtT20/D16v cells and demonstrate that somatostatin inhibits stimulated ACTH release by these cells. Equilibrium binding studies with [125I]Tyr1]somatostatin showed the presence of a single class of noninteracting binding sites on AtT20/D16v cells. Half-maximal binding of somatostatin occurred at 1.7 X 10(-9) M, and there were 26,300 binding sites/cell. The binding of [125I]Tyr1]somatostatin was not significantly inhibited by the hypothalamic peptides TRH, LHRH, and substance P. Somatostatin had no consistent effect on basal ACTH secretion by AtT20/D16v cells, but it inhibited ACTH secretion stimulated with either 50 mM KCl or a hypothalamic extract. Half-maximal inhibition occurred with 4 X 10(-10) M somatostatin. TRH, LHRH, and substance P at concentrations of 10(-7) M were without effect. Somatostatin had no effect on either basal or stimulated hormone secretion by GH12C1 or F4C1 cells, two cell strains which lack specific somatostatin-binding sites. A critical concentration of extracellular calcium was required for the stimulation of ACTH secretion in AtT20/D16v cells. No response to 50 mM KCl occurred in the presence of EGTA or cobalt. Increased extracellular calcium overcame the inhibition of stimulated hormone secretion by EGTA, cobalt, and somatostatin. Therefore, we conclude that the inhibition of stimulated ACTH secretion by somatostatin involves the interaction of the peptide with specific binding sites on AtT20/D16v cells and the inhibition of stimulus-elicited calcium influx.
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PMID:Inhibition of adrenocorticotropin secretion by somatostatin in pituitary cells in culture. 610 20

Th effects on ganglion cell light responses and spontaneous activity of neurotransmitter candidates, applied by nebulizer spray and iontophoresis, were studied in the isolated carp retina. ACh, GABA, and substance P had strong effects on the ganglion cells; dopamine and the amino acids aspartate, glutamate, and glycine and only weak effects. ACh and substance P exerted their actions even when synaptic transmission was blocked by cobalt chloride, suggesting postsynaptic receptors for those agents on the ganglion cell membrane. The 3 amino acids and dopamine do not appear to act directly on the ganglion cells. The pharmacological sensitivity of ganglion cells was correlated with their physiological response type. About three-quarters of ON/OFF and half of other transiently responding ganglion cells were excited by micromolar concentrations of cholinergic agonists; most ON-center sustained ganglion cells were insensitive. The light response of some of the ACh-sensitive cells could be suppressed by cholinergic antagonists. Substance P generally excited ganglion cells with an ON-component in their light response. GABA inhibited cells of all response types, but affected least the OFF-center tonic cells. In view of these observations, and of corroborating histological evidence, we propose that ACh, GABA, and substance P are neurotransmitters that are released by amacrine cells and affect receptors located on ganglion cells.
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PMID:Inner plexiform circuits in the carp retina: effects of cholinergic agonists, GABA, and substance P on the ganglion cells. 617 85

Substance P-like immunoreactivity was examined in the Limulus lateral eye and photocerebrum by the unlabeled antibody peroxidase-antiperoxidase method. Small-diameter immunoreactive fibers innervate the corneal epidermis of the lateral eye and appear to be part of a generalized epidermal innervation. No immunoreactive neurons or fibers were found in the ventral, median, or lateral optic nerves nor in the lamina or chiasma. The optic medulla contains neurons with immunoreactive perinuclear caps in the ganglion cell layer and fibers of undetermined origin in the posterolateral regions of the neuropil. The central body contains many immunoreactive fibers in its neuropil, some or all of which arise from neurons adjacent to its anteromedial tips. Immunoreactive neurons within the curve of the central body give rise to processes which join the central neuropil of the photocerebrum. The immunoreactive innervation of the corpora pedunculata includes processes which terminate amont Kenyon cell somata, and processes in the peduncular neuropil, all of which arise from a bilateral cluster of neurons along the midline. Attempts to investigate the source of the immunoreactive fibers using cobalt impregnation of the severed circumesophageal connective have revealed two additional innervations of the corpora pedunculata, one from raphe neurons along the midline and one from lateral portions of the midline ganglion adjacent to but separate from that portion containing the immunoreactive neurons. The results demonstrate that immunocytochemical methods are another powerful tool for the study of neuronal pathways in invertebrates.
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PMID:Neuropeptide immunoreactivity in Limulus. I. Substance P-like immunoreactivity in the lateral eye and photocerebrum. 618 Nov 6

Preganglionic neurons in the lower lumbar spinal cord were labeled with horseradish peroxidase applied to the cut ends of the intermesenteric trunk in golden hamsters. A black granular reaction product was obtained in HRP-labeled cells by soaking spinal cord tissue in a cobalt chloride solution prior to treatment with diaminobenzidine (DAB) and hydrogen peroxide. Spinal cord sections containing labeled preganglionic neurons were processed with the immunoperoxidase (PAP) technique. Immunoreactive processes appeared as rust-brown beads. Concentrations of beaded processes exhibiting enkephalin-like, substance P-like (SPI) and somatostatin-like (SOMI) immunoreactivity were present around HRP-labeled preganglionic neurons in the intermediolateral cell column and in the dorsal commissural nucleus. Immunoreactivity was also present in the superficial dorsal horn, the dorsolateral funiculus and around the central canal. A prominent fiber system exhibiting SPI and SOMI extended from the ventral white matter to the ventral horn.
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PMID:Leu-enkephalin, substance P, and somatostatin immunohistochemistry combined with the retrograde transport of horseradish peroxidase in sympathetic preganglionic neurons. 618 92

1. Substance P (SP) induces histamine release from isolated rat peritoneal mast cells at concentrations of 0.1-10 muM.2. Inhibitors of glycolysis and oxidative phosphorylation prevent the release of histamine induced by SP.3. Cells heated to 47 degrees C for 20 min release histamine when treated with an agent causing cell lysis but fail to release in response to SP.4. SP does not release histamine by interacting with cell-bound IgE.5. Histamine release by SP is rapid, with more than 90% of the response occurring within 1 min of the addition of the peptide to mast cells at 37 degrees C.6. Substance P, unlike antigen-antibody or compound 48/80, does not show enhanced release of histamine when calcium (0.1-1 mM) is present in the extracellular medium but calcium increases the response to SP when the ion is added after the peptide. Extracellular calcium (0.1-1 mM), magnesium (1-10 mM) and cobalt (0.01-0.1 mM) all inhibit SP-induced histamine release when added before the peptide. Pre-treatment of the cells with EDTA (10 mM) and washing in calcium-free medium inhibits the histamine release induced by SP.7. Histamine release induced by SP was optimum at an extracellular pH of 7.2.8. A number of peptides structurally related to SP were examined for histamine-releasing activity. At the concentrations tested, the N-terminal dipeptides Lys-Pro and Arg-Pro, tuftsin, physalaemin, eledoisin, SP(3-11), SP(4-11) and [p-Glu(6), p-amino Phe(7)]-SP(6-11) were all found to be inactive. The relative activities of the other peptides were: [Formula: see text]9. Rat basophilic leukaemia cells (RBL-2H3) fail to respond to SP at concentrations which activate rat mast cells. Release of 5-hydroxytryptamine by immunological activation of RBL cells is not changed by the presence of SP.10. The mechanism of action of SP on mast cells and the nature of the SP receptor on mast cells is discussed in relation to SP receptors in other cell types.
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PMID:The effects of substance P on histamine and 5-hydroxytryptamine release in the rat. 618 68

1. The transient release of 86Rb from parotid slices induced by secretagogues was investigated. 2. In the absence of external Ca, only one transient response (to carbachol) could be obtained. 3. After blocking the cholinergic stimulus with atropine, a second response (to substance P) could be elicited if the slices were briefly (2 min) exposed to a Ca-containing medium. 4. The magnitude of the substance P response depended on the concentration of Ca to which the slices had been exposed. 5. An exposure to Ca of 2 min duration was found to be sufficient to restore maximal substance P responsiveness. 6. These results are interpreted to mean that the cholinergic stimulus elicited a transient 86Rb efflux response by first releasing a finite pool of cellular Ca which could be reloaded from the extracellular space by a brief (2 min) incubation in a Ca-containing medium. The magnitude of the subsequent response to substance P apparently reflects the quantity of Ca taken up by the pool. 7. A number of cationic substances antagonized the restoration by Ca of the substance P response; the rank order of potency was: La3+ = Tm3+ greater than Co2+ = Ni2+ greater than neomycin much greater than Mg2+. 8. These same substances were examined for their relative abilities to inhibit Ca binding to phosphatidylinositol-4, 5-bisphosphate; in this case the rank order of potency was: La3+ = Tm3+ greater than neomycin greater than Co2+ greater than Ni2+ = Mg2+. 9. It is concluded that the uptake process does not appear to reflect Ca binding to phosphatidylinositol-4, 5-bisphosphate.
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PMID:Nature of the receptor-regulated calcium pool in the rat parotid gland. 618 69

1. The depressant actions of Mg2+ and a range of other divalent ions on synaptic excitation and on responses produced by excitatory amino acids and other putative transmitters have been investigated in hemisected isolated spinal cords of frogs and neonatal rats. Some comparative studies were also made using the rat isolated superior cervical ganglion. 2. At concentrations above 10 microM, Mg2+ selectively antagonized N-methyl-D-aspartate (NMDA)-induced motoneurone depolarization as recorded from ventral roots of tetrodotoxin-blocked spinal cords. Depolarization evoked by quisqualate (unaffected by 20 mM-Mg2+) was resistant to the depressant action of these ions, while depolarizations evoked by other excitant amino acids were depressed to intermediate degrees. 3. Mn2+, Co2+ and Ni2+ had qualitatively similar actions to Mg2+; Mn2+ was somewhat less potent and Co2+ and Ni2+ more potent than Mg2+. The alkaline earth metal ions, Ca2+, Sr2+ and Ba2+, had very weak Mg2+-like actions. Ca2+ and Mg2+ acted additively in depressing amino acid-induced responses. 4. Mg2+ also depressed motoneurone responses evoked by noradrenaline, substance P and carbachol in the neonatal rat isolated spinal cord. However, none of these effects were as marked as the depression of NMDA-induced responses by Mg2+ in this preparation. Mg2+ did not depress motoneurone depolarization produced by 5-HT in the rat spinal cord or the depolarizing action of GABA on primary afferent terminals of the isolated frog spinal cord. 5. At concentrations producing marked depression of NMDA-induced responses, Mg2+ also depressed synaptic transmission in spinal cords in the absence of an effect on ganglionic transmission. At the same concentrations, Mn2+, Co2+ and Ni2+ depressed synaptic transmission in both preparations. 6. From the similarity in action between Mg2+ and the D-alpha-aminoadipate group of NMDA antagonists, it is suggested that the central depressant action of low concentrations of Mg2+ involves predominantly a postsynaptically mediated interference with the action of an excitatory amino acid transmitter.
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PMID:Selective depression of excitatory amino acid induced depolarizations by magnesium ions in isolated spinal cord preparations. 625 39

Secretory vesicles isolated from the neural and intermediate lobes of the bovine pituitary contained a membrane-bound aminopeptidase activity which cleaved arginine from beta-LPH60-65 (Arg-Tyr-Gly-Gly-Phe-Met) and Arg-MCA. Neither methionine enkephalin (Tyr-Gly-Gly-Phe-Met) nor Substance P, which has an N-terminal arginine followed by a proline, could serve as substrates for this aminopeptidase activity; nor could cathepsin B-like or chymotrypsin-like enzyme activities be detected in the vesicle preparations. Maximal enzyme activity was at pH 6.0, and the activity was inhibited by EDTA, stimulated by Co2+ and Zn2+, but was unaffected by leupeptin, pepstatin A, phenylmethylsulfonyl fluoride and p-chloromercuribenzenesulfonate, suggesting that the enzyme is a metalloaminopeptidase. The presence of this aminopeptidase activity in secretory vesicles suggests that it may be involved in peptide prohormone processing.
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PMID:An aminopeptidase activity in bovine pituitary secretory vesicles that cleaves the N-terminal arginine from beta-lipotropin60-65. 643 44

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