Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P20366 (substance P)
 21,176 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The effect of intrathecally (i.t.) applied tachykinin antagonist D-NicLys1, 3-Pal3, D-Cl2Phe5, Asn6, D-Trp7.9, Nle11-substance P (SP), spantide II, on the nociceptive flexor reflex was studied in decerebrate, spinalized, unanaesthetized rats over the dose range of 10 ng-10 micrograms. I.t. spantide II usually caused weak facilitation of the flexor reflex, especially at lower doses (10-100 ng) and at higher doses (1-10 micrograms) it sometimes depressed the reflex. Pre-treatment with spantide II (1, 3 or 10 micrograms) effectively antagonized the facilitatory effect of 10 ng i.t. SP on the flexor reflex for about 30 min. The facilitation of the reflex induced by i.t. administration of other neuropeptides present in primary afferents, somatostatin (SOM), vasoactive intestinal peptide (VIP), calcitonin gene-related peptide (CGRP) and galanin (GAL), was not influenced by spantide II. This non-toxic antagonist also effectively blocked facilitation of the flexor reflex induced by C-fiber conditioning stimulation of the sural nerve. The present results indicate that spantide II is an effective and specific tachykinin antagonist in the spinal cord. Furthermore, C-fiber stimulation facilitates the nociceptive flexor reflex through a mechanism involving the release of SP from the central terminals of primary afferents.
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PMID:The specific antagonistic effect of intrathecal spantide II on substance P- and C-fiber conditioning stimulation-induced facilitation of the nociceptive flexor reflex in rat. 170 83

Release of [3H]acetylcholine ([3H]ACh) was examined in a submucous plexus preparation obtained from the guinea pig small intestine in vitro. Constant-current field stimulation evoked ACh output; this output was dependent on the stimulus frequency applied. Maximal release was observed at 10 Hz; this release was blocked by tetrodotoxin (1 x 10(-6) M) or in Ca2(+)-free buffer. Serotonin [5-hydroxytryptamine (5-HT)] stimulated the release of ACh dose dependently, with an ED50 of 5 x 10(-7) M. Substance P was ineffective, while vasoactive intestinal peptide weakly stimulated ACh secretion. Several neuropeptides were tested on their ability to modulate 5-HT-evoked ACh release. Dynorphin A inhibited 5-HT-stimulated ACh release, while Met-enkephalin was without any effect. Both somatostatin and galanin were effective modulators, with an inhibitory effect in the submicromolar range and an excitatory effect at higher concentrations. The response characteristics of the cholinergic neurons of submucosal plexus differ markedly from those of the myenteric plexus. These distinct features form an important framework for future functional studies on submucous plexus neurons.
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PMID:Modulation of submucosal cholinergic neurons by 5-hydroxytryptamine and neuropeptides. 170 72

A study in cats has shown that intracameral injection of calcitonin gene-related peptide (CGRP) increases the outflow facility by four- to fivefold concomitant with a decrease in intra-ocular pressure (IOP). Since there are great differences in the anatomy of the aqueous outflow routes between cats and primates, we have examined the effects of CGRP in the cynomolgus monkey. The possible influence of the sensory neuropeptides cholecystokinin (CCK), galanin and substance P on the outflow facility and IOP were also investigated. Determinations were performed using a two-level constant-pressure procedure. At 40-60 min after intracameral injection of 3 micrograms CGRP the outflow facility was increased from 0.68 +/- 0.11 to 1.03 +/- 0.15 microliters min-1 mmHg-1 in the CGRP-treated eyes, and from 0.71 +/- 0.12 to 0.79 +/- 0.10 microliter min-1 mmHg-1 in the control eyes. The mean difference in increase was 0.27 +/- 0.06 microliter min-1 mmHg-1 (P less than 0.01, n = 7). During the experiments there was a small rise in the IOP. CGRP at a dose of 3 micrograms caused a small rise in aqueous humor protein concentration. An attempt to release endogenous CGRP with capsaicin did not result in an increased outflow facility. Three micrograms each of CCK, galanin and substance P had no significant effect on either the outflow facility or the IOP. A miosis was observed in the experiments with CCK in agreement with previous findings. CCK seems thus to cause contraction of the pupillary sphincter but does not influence the ciliary muscle sufficiently to cause a facility effect in the monkey eye.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Outflow facility in the monkey eye: effects of calcitonin gene-related peptide, cholecystokinin, galanin, substance P and capsaicin. 170 89

The presence of several neuropeptides (neuropeptide Y (NPY), vasoactive intestinal polypeptide (VIP), calcitonin gene-related peptide (CGRP), substance P (SP), galanin (GAL), enkephalin (ENK), somatostatin (SOM) was established in the early pregnant human cervix using indirect immunofluorescence immunohistochemistry. Several peptides (VIP, NPY, CGRP, GAL) were present both in free nerves among smooth muscle cells and around blood vessels. Others (SP, SOM) were only seen as single varicosities among smooth muscle cells. Randomized treatment of patients with RU 486 (mifepristone) prior to surgical sampling revealed no clearcut differences in peptide immunoreactivities. After RU 486 treatment, however, there was a tendency towards a decrease of NPY- and VIP-immunoreactivity, and an increase of CGRP-immunoreactivity.
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PMID:Peptide-containing nerves in the human pregnant uterine cervix: an immunohistochemical study exploring the effect of RU 486 (mifepristone). 170 49

Addition of the neuropeptide galanin to small cell lung cancer (SCLC) cells loaded with the fluorescent Ca2+ indicator fura-2-tetraacetoxymethylester causes a rapid and transient increase in the intracellular concentration of Ca2+ ([Ca2+]i) followed by homologous desensitization. Galanin increased [Ca2+]i in a concentration-dependent fashion with half-maximum effect (EC50) at 20-22 nM in H69 and H510 SCLC cells. Galanin mobilized Ca2+ from intracellular stores since its effects on [Ca2+]i were not blocked by chelation of extracellular Ca2+. Pretreatment with pertussis toxin (200 ng/ml for 4 h) did not prevent galanin-induced Ca2+ mobilization. In contrast, direct activation of protein kinase C with phorbol esters attenuated the Ca2+ response induced by galanin. The effects of galanin could be dissociated from changes in membrane potential: galanin did not increase membrane potential in SCLC cells loaded with bis(1,3-diethyltiobarbiturate)-trimethineoxonol and induced Ca2+ mobilization in depolarized SCLC cells, i.e., in cells suspended in a solution containing 145 mM K+ instead of Na+. Galanin also caused an increase in the formation of inositol phosphates in a time- and dose-dependent manner (EC50 10 nM). A rapid increase in the inositol trisphosphate fraction was followed by a slower increase in the inositol monophosphate fraction. Galanin stimulated clonal growth of both H69 and H510 cells in semisolid (agarose-containing) medium. This growth-promoting effect was sharply dependent on galanin concentration (EC50 20 nM) and markedly inhibited by [Arg6,D-Trp7,9,MePhe8]substance P, a recently identified broad spectrum neuropeptide antagonist. The results show for the first time that galanin receptors are coupled to inositol phosphate and [Ca2+]i responses in SCLC cells and, in particular, that this neuropeptide can act as a direct growth factor for these human cancer cells.
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PMID:Galanin stimulates Ca2+ mobilization, inositol phosphate accumulation, and clonal growth in small cell lung cancer cells. 170 78

The arrangement of the enteric nerve plexuses in the colon of the guinea-pig and the distributions and projections of chemically specified neurons in this organ have been studied. Immunoreactivity for neuron specific enolase was used to examine the total population of neurons and individual subpopulations were studied using antibodies raised against calbindin, calcitonin gene-related peptide (CGRP), leu-enkephalin, gastrin releasing peptide (GRP), galanin, gamma aminobutyric acid, neurokinin A, neuropeptide Y (NPY), somatostatin, substance P, tyrosine hydroxylase and vasoactive intestinal peptide (VIP). Neuronal pathways within the colon were lesioned using myotomy and myectomy operations and extrinsic pathways running between the inferior mesenteric ganglia and the colon were also severed. Each of the antibodies revealed nerve cells and nerve fibres or only nerve fibres within the wall of the colon. VIP, galanin and GRP were in anally projecting pathways in the myenteric plexus, as they are in other species. In contrast, there are differences in the projection directions of enkephalin, substance P, NPY and somatostatin nerve fibres between regions and species. Surprisingly, somatostatin and NPY fibres have opposite projections in the small intestine and colon of the guinea-pig. The majority of nerve fibres that innervate the circular muscle, including fibres with immunoreactivity for VIP, enkephalin, substance P, NPY, galanin and GRP come from the myenteric ganglia. The mucosa is innervated by fibres from both the myenteric and submucous ganglia. The present results suggest that the guinea-pig distal colon is a suitable place in which to determine relations between structure, neurochemistry and functions of enteric neural circuits.
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PMID:Projections of chemically-specified neurons in the guinea-pig colon. 170 5

A search for neuropeptide nerves in the healing of the experimentally ruptured medial collateral ligament (MCL) of the rabbit knee used specific antisera to the neuropeptides Substance P, calcitonin gene-related peptide (CGRP), and galanin. Sutured and unsutured MCLs were studied four and 14 weeks postoperatively. Both fluorescent thin nerve strands and small dotlike nerve terminals were regularly seen in the healing zone and in the adjacent normal ligamentous tissue, suggesting innervation of such structures by neuropeptide nerves. All three neuropeptides were more abundant in sutured ligaments than in unsutured ligaments, which may suggest beneficial effects of the apposition of the torn ligament ends on local nerve regeneration. Active involvement of the neural elements in the healing process was also suggested by kinetic studies showing a decrease in Substance P and CGRP staining as well as an increase in galanin staining during the study period. These changes in the periphery parallel the reactive changes earlier described in the dorsal root ganglion and dorsal horn cells occurring after a peripheral nerve injury. This may depend on the antidromic transport to the periphery of neuropeptides synthesized in the central nervous system. This experimental neuroimmunohistochemical mapping study and the known effects of neuropeptides on blood vessels, macrophages, and fibroblasts should stimulate further work on the role of innervation in ligamentous healing.
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PMID:Immunoreactive neuropeptides in nerves in ligamentous tissue. An experimental neuroimmunohistochemical study. 170 72

The peptides galanin (GAL), substance P (SP), and calcitonin gene-related peptide (CGRP) were analyzed with immunohistochemistry and radioimmunoassay in the spinal cord, dorsal root ganglia, dorsal roots, and sciatic nerve of normal rats and rats subjected to several experimental procedures, including ligation, crush, and/or sectioning of nerves. The results show that peripheral nerve transection induces a dramatic increase in GAL content both in dorsal roots and sciatic nerve, demonstrating that this lesion causes an increased out-transport of the newly synthesized peptide both into the central and peripheral branches of the primary sensory neurons. In contrast evidence was obtained for decreased out-transport of SP and CGRP. The functional significance of these findings remains to be analyzed.
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PMID:Further studies on galanin-, substance P-, and CGRP-like immunoreactivities in primary sensory neurons and spinal cord: effects of dorsal rhizotomies and sciatic nerve lesions. 170 68

The effect of focused high energy microwave treatment (MW) on brain concentrations and molecular forms of substance P, neurokinin A, neuropeptide Y, neurotensin, galanin and calcitonin gene-related peptide was investigated. Groups of rats were treated as follows: 1) MW, storage for 60 min at 22 degrees C, 2) Decapitation, storage for 60 min at 22 degrees C. 3) Decapitation, storage for 60 min at 22 degrees C, MW treatment, 4) MW, decapitation, storage for 2 min at 22 degrees C and 5) Decapitation, storage for 2 min at 22 degrees C. Peptide concentrations were in all instances highest in the MW sacrificed groups. MW increased the concentration of intact peptides by rapid inhibition of peptidase activity and increase in peptide solubility/extractability.
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PMID:Microwave irradiation increases recovery of neuropeptides from brain tissues. 170 37

Immunocytochemical methods have been used to examine the localisation of 3 neurofilament proteins and the calcium binding protein, calbindin D28k, in whole mount preparations of the submucous plexus in the Wistar rat. Neurofilament-M (160 kDA protein) was present in 40% of the submucosal neurons, staining fine filaments in the soma and the axonal processes. Calbindin D28k was present in 40% of the submucosal neurons staining both the soma and nerves within the plexus. The neurofilament proteins and calbindin D28k were never observed within the same neurons. Neurofilament-M was co-localised with substance P and calcitonin gene-related peptide but not somatostatin or the other neuropeptides investigated. Calbindin D28k was co-localised with vasoactive intestinal polypeptide and neuropeptide Y. Galanin- and somatostatin-immunoreactive neurons did not contain either the neurofilament proteins or calbindin D28k. The results demonstrate the presence of subsets of submucosal neurons that can be distinguished by the presence of neurofilament-M or calbindin D28k.
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PMID:Neurofilament M and calbindin D28k are present in mutually exclusive subpopulations of enteric neurons in the rat submucous plexus. 170 5


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