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

The topographical distribution of neuropeptide-containing cell bodies, fibers and terminals was studied in human parabrachial nuclei and the pontine tegmentum with immunohistochemical stainings. Brains of seven adult human subjects of 35-72 years were fixed within 2 h post mortem. Serial sections were immunostained by antisera of 14 different neuropeptides--oxytocin, vasopressin, thyrotropin-releasing hormone, angiotensin II, calcitonin gene-related peptide, beta-endorphin, dynorphin A, dynorphin B, leucine-enkephalin, alpha-melanocyte stimulating hormone, substance P, neuropeptide Y, cholecystokinin and galanin--alternately. All of these peptides were found to be present in nerve fibers and terminals, but only two, angiotensin II and dynorphin B, in cell bodies of the parabrachial nuclei. Calcitonin gene-related peptide-, neuropeptide Y-, cholecystokinin- and galanin-immunoreactive cells were present in other areas of the pontine tegmentum, like the motor trigeminal nucleus, locus coeruleus, periventricular gray matter but not in the parabrachial nuclei. Peptidergic fibers were distributed unevenly throughout the pontine tegmentum having unique, individual distribution patterns. In the parabrachial nuclei, substance P, neuropeptide Y, cholecystokinin and galanin showed the highest density of immunoreactive neuronal networks. Moderate to low concentrations of immunoreactive processes were detected by calcitonin gene-related peptide, alpha-melanocyte stimulating hormone, dynorphin B, thyrotropin releasing hormone, leucine-enkephalin, dynorphin A, angiotensin II, beta-endorphin, vasopressin and oxytocin antisera, respectively. Other pontine tegmental areas, like the locus coeruleus, dorsal tegmental, pontine raphe and motor trigeminal nuclei as well as the central gray of the tegmental region exhibited a varying assortment of neuropeptides with distinct, individual localization patterns. Their detailed topographical distributions are mapped and given in coronal sections.
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PMID:Immunohistochemical study on the distribution of neuropeptides within the pontine tegmentum--particularly the parabrachial nuclei and the locus coeruleus of the human brain. 154 21

The neuropeptidergic innervation of the normal and obstructed human pyeloureteral junction was investigated using immunohistochemical techniques. A dense innervation of neuropeptide Y (NPY) and vasoactive intestinal polypeptide (VIP) in the intrinsic obstruction type was demonstrated. NPY and VIP formed networks in the muscular layer. NPY was also found in perivascular plexuses and VIP adjacent to the epithelium. Calcitonin gene-related peptide, galanin and substance P nerves were also seen in the muscular layer, although sparsely. It is proposed that NPY and VIP have a role in the pathophysiology of the intrinsic obstruction type of the human pyeloureteral junction. The innervation pattern of the junction with the external type of obstruction was similar to that of the normal pyeloureteral junction.
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PMID:Peptidergic innervation of the normal and obstructed human pyeloureteral junctions. 159 31

These studies of cluster headache (CH) focus on two key features of pain transmission: a) sensory nerves when stimulated, as well as the expected afferent transmission, also display an efferent function which affects capillaries, glands, and smooth muscle (of the iris in CH); substance P (SP) and allied transmitters such as Vasoactive Intestinal Peptide (VIP) and Calcitonin Gene-Related Peptide (CGRP) are the main agonists of this dual afferent-efferent function; b) impaired pain transmission (deafferentation-like condition) provokes a rostral spread of neuronal irritability and automatic firing ("quasi epileptic foci") producing a clinical predilection for pain with the generation of "spontaneous" pains along the sensory pathways. The substrates studied in the present experiments are the iris, salivary glands, and nasal mucosa. 1) Iris: the conjunctival instillation of SP induces isocoric miosis both in CH sufferers and in normals, thus excluding gross SP receptoral dysfunction of the iris muscle in CH. Electrical stimulation of extraocular (infratrochlear) endings of the first branch of the trigeminal nerve provokes a miosis, which is significantly less in the symptomatic eye than in the contralateral one. This miosis is ascribed to a retrograde release of SP, induced by electrical stimulation of the trigeminal ophthalmic branch. The relatively poor miosis in the painful eye could correlate with a deficient release of SP from the sensory terminals in the iris. 2) Salivary glands: an increase of substance P-like immunoreactivity is found in the saliva taken from the asymptomatic side, but not from the painful side during a cluster headache attack, thus showing at this level also an asymmetry as previously shown in other head structures. 3) Nasal mucosa: intranasal application of capsaicin, a powerful releaser of SP from sensory terminals, evokes an immediate burning pain in the ipsilateral nasal, ocular, and temporal areas, as well as lacrimation and rhinorrhea. A gradual decrease (tachyphylaxis) of these phenomena is consistently observed after few days of daily nasal administration of capsaicin. When this treatment is applied to CH patients, a rapid decrease in the number and intensity of attacks, and even disappearance of symptoms accompanies the decline of the capsaicin-induced manifestations. Local (nasal) capsaicin, in spite of evoking immediately the same vegetative (rhinorrhea, lacrimation, conjunctival congestion) and in part nociceptive (transient nasal, ocular, temporal burning) phenomena of CH, never has been able to provoke delayed spontaneous-CH like attacks. Such delayed provoked attacks, one of the most pregnant phenomena in CH investigations, are almost constantly evoked by systemic stimuli.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Substance P theory: a unique focus on the painful and painless phenomena of cluster headache. 168 82

Calcitonin gene-related peptide (CGRP)-like immunoreactivity was localized immunocytochemically in the large motoneurons in the ventral horn of rat spinal cord. Using fluorescence double-labelling substance P (SP)-immunoreactive nerve fibres were found to surround both the CGRP-positive and negative motoneurons, whereas enkephalin (ENK)-immunoreactive fibres surrounded mainly CGRP-negative cells. All CGRP-like immunoreactive motoneurons were also choline acetyltransferase (ChAT)- and acetylcholinesterase (AChE)-positive. On the other hand a large population of ChAT- and AChE-positive motoneurons were devoid of CGRP-immunoreactivity. It is probable that CGRP/ChAT/AChE-positive cells surrounded by SP-positive fibres have different functions in motoric nervous system than the CGRP-negative ChAT/AChE-positive cells, which are surrounded by ENK-immunoreactive fibres.
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PMID:Immunocytochemical study of the relations of acetylcholinesterase, enkephalin-, substance P-, choline acetyltransferase- and calcitonin gene-related peptide-immunoreactive structures in the ventral horn of rat spinal cord. 169 14

Nerves within and under the esophageal epithelium of the opossum esophagus were investigated morphologically with osmication and immunohistochemically for ten neuropeptides. The structurally similar but functionally diverse epithelia of the anal canal and snout skin, on which no immunohistochemical information exists, were similarly investigated for comparison. Total innervation was estimated from osmication, which revealed intraepithelial nerves in all three tissues in the following order of density: snout skin greater than anal canal greater than esophagus. Calcitonin gene-related peptide and substance P occurred in all three organs. The snout skin had intraepithelial galanin nerves but not vasoactive intestinal polypeptide, while conversely the esophagus and anal canal had vasoactive intestinal polypeptide but not galanin. All peptides found intraepithelially also occurred subepithelially. Calcitonin gene-related peptide, galanin, neuropeptide Y, substance P and vasoactive intestinal polypeptide subepithelial nerves occurred in all the tissues, while gastrin releasing peptide nerves occurred infrequently in the subepithelial regions of the esophagus and anal canal, but not the snout skin. As these epithelia neither secrete nor absorb, their nerves are presumably sensory. The peptides investigated could not account for all intraepithelial nerves demonstrated by osmium. Differences in the innervation of these epithelia may result from their differing sensory requirements.
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PMID:Mucosal peptidergic innervation of the opossum esophagus and anal canal: a comparison with snout skin. 169 56

The distribution and localization of several neuropeptides were investigated in the lichenified lesions of 11 patients with atopic dermatitis using indirect immunofluorescence. Substance P-positive nerve fibres were observed in most of the cases of atopic dermatitis, but not in normal controls. Somatostatin immunoreactive nerves were not found in the skin of atopic dermatitis, whereas a normal pattern of immunoreactivity could be detected in most of the healthy subjects. Neuropeptide Y-positive dendritic epidermal cells were observed in lesional skin from patients with atopic dermatitis, but not in controls. Calcitonin gene-related peptide and vasoactive intestinal polypeptide immunoreactivity in patients with atopic dermatitis did not differ from that in healthy subjects. With galanin antiserum a diffuse intracellular staining was observed in the epidermis of both atopic patients and controls, while no positive staining was found with either neurotensin or neurokinin A antibodies in either group. These findings suggest a possible involvement of some neuropeptides in the pathomechanisms of atopic dermatitis.
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PMID:Neuropeptides in skin from patients with atopic dermatitis: an immunohistochemical study. 169 5

The effects of long-term treatment with the laxatives senna and 1,8-dihydroxyanthraquinone (danthron) were investigated in isolated mesenteric vascular beds of rats. The senna was administrated as ground senna pods mixed with milk chocolate. Danthron was also administered in this way. Chocolate-fed, senna-fed, and danthron-fed rats were supplied with usual feed, supplemented with chocolate, chocolate adulterated with ground senna pods, and chocolate adulterated with danthron, respectively. A group of control rats had no supplement. Perivascular nerve stimulation elicited frequency-dependent vasoconstriction of the mesenteric bed. There were no significant differences in responsiveness to perivascular nerve stimulation among mesenteric beds from the four groups. During two separate consecutive applications of capsaicin, a sensory neurotoxin, pressor responses to nerve stimulation of vascular beds from the control and chocolate-fed rats were inhibited on both occasions. However, in mesenteric beds from the senna-fed and danthron-fed groups, inhibition of pressor responses was the same on the first application of capsaicin as in the control and chocolate-fed groups, but the effect of the second application of capsaicin was greatly reduced. Calcitonin gene-related peptide, adenosine 5'-triphosphate, and adenosine mimicked the inhibitory action of capsaicin on nerve stimulation in all groups, while substance P was without effect. There was no significant difference in responsiveness to these agents among the four groups. These results suggest that senna or its metabolites may cause a sensory neuropathy of mesenteric resistance vessels and that calcitonin gene-related peptide, adenosine 5'-triphosphate, and adenosine, but not substance P, are possible candidates as mediators of the inhibitory effects induced by capsaicin.
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PMID:Effects of long-term laxative treatment on rat mesenteric resistance vessel responses in vitro. 169 84

Using in vivo microdialysis in the dorsal spinal cord of the rat, we have previously observed increases in glutamate and aspartate during exposure to a noxious stimulus. The present investigation was designed to determine whether these increases may be mediated by substance P. Infusion of 1 mM of substance P in the dialysis fluid increased the concentrations of glutamate and aspartate, similar to the response seen during noxious stimulation. In addition, substance P also increased the concentrations of the inhibitory amino acids glycine and taurine. Calcitonin gene-related peptide, previously shown to enhance substance P-induced biting and scratching behavior, produced no effect on amino acid release by itself but potentiated the apparent release of taurine by substance P. To assess the importance of substance P-induced amino acid release in sensory processing, we examined the influence of taurine and of excitatory amino acid antagonists on the biting and scratching behavior produced by excitatory amino acids and substance P. Taurine selectively inhibited only substance P-induced biting and scratching while excitatory amino acid antagonists inhibited only excitatory amino acid-induced behavior. To further explore the ability of taurine to inhibit the substance P-induced behavior, 3 tests of nociception were then used. Pretreatment with taurine inhibited the nociceptive-related writhing behavior produced by an intraperitoneal injection of acetic acid in mice but failed to alter the latency of response in the hot plate or tail flick assay.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Interactions between substance P, calcitonin gene-related peptide, taurine and excitatory amino acids in the spinal cord. 170 Mar 56

Histochemical and pharmacological studies were performed on the rabbit central ear artery. In perivascular nerves, positive immunoreactivity for calcitonin gene-related peptide and substance P was demonstrated. Calcitonin gene-related peptide-like immunoreactivity was also found to be colocalised with substance P-like immunoreactivity in a subpopulation of perivascular nerves. In vitro incubation with 6-hydroxydopamine did not alter the intensity and/or density of either the calcitonin gene-related peptide- or substance P-like immunoreactive fibres, whereas incubation with capsaicin significantly reduced both. In pharmacological studies, calcitonin gene-related peptide reduced the vasoconstrictor responses to exogenous noradrenaline and alpha, beta-methylene ATP and to electrical field stimulation in a concentration-dependent manner. In segments of the central ear artery preconstricted with noradrenaline, relaxation mediated by calcitonin gene-related peptide was endothelium-independent. These results shed new light on the innervation and nervous control of the rabbit central ear artery previously thought to be exclusively under sympathetic (adrenergic and purinergic) control. Further, the results suggest that calcitonin gene-related peptide localised in sensory nerves in the rabbit central ear artery may act as an inhibitory modulator of excitatory sympathetic vascular neurotransmission.
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PMID:Sensory-motor neuromodulation of sympathetic vasoconstriction in the rabbit central ear artery. 170 78

Substance P and somatostatin may be transmitters of nociceptive information, which are involved in the transmission of pressure and heat nociceptive information, respectively, in the spinal dorsal horn. Calcitonin gene-related peptide, which is present in the primary sensory neurons having substance P or somatostatin, may function as a pain-promoting substance and be involved in the production of inflammation-induced hyperalgesia. The descending noradrenergic system plays a role in inhibiting nociceptive transmission in the spinal dorsal horn, and inhibits the release of substance P evoked by noxious mechanical stimulation. Persistent noxious stimuli increase the release of Met-enkephalin from the nucleus reticularis gigantocellularis, which promotes the activity of the descending noradrenergic system. Morphine activates the descending noradrenergic system, acting on the nucleus reticularis gigantocellularis. Morphine also activates the descending serotonergic system, which inhibits the release of somatostatin evoked by thermal noxious stimulation.
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PMID:[Neuropeptide-mediated transmission of nociceptive information and its regulation. Novel mechanisms of analgesics]. 170 78


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