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 vestibular end organs of the rabbit were fixed intracardially with phosphate buffered 4% formaldehyde, sectioned for 15 micron cryostat sections and incubated with monoclonal substance P (SP) antibody. Specific SP-like immunoreactivity (SPLI) was observed within and below the sensory epithelia of both utricular and saccular maculae and ampullary cristae. Particularly strong SPLI was seen in the maculae which showed many SPLI-positive axons in the subepithelial space and a network of SPLI-positive structures in the basal zones of the sensory epithelium. The calyceal terminals of type I hair cells showed regularly SPLI. The possibility of a transmitter or modulator role for SP in the vestibular function is suggested.
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PMID:Is substance P the neurotransmitter in the vestibular end organs? 620 37

When samples of the ventricle surfaces of human post-mortem brain were examined by scanning- and transmission electron microscopy, varicose nerve fibres could be seen traversing among the cilia and microvilli of ependymal cells. The varicosities contained numerous small electron-lucent vesicles and frequent large electron-dense vesicles, and were usually nonsynaptic but occasionally anchored to the surface by desmosome-like junctions. Supra-ependymal nerve fibres were observed in the lateral ventricles (e.g., n. caudatus), foramen of Monro (stria medullaris), third ventricle (habenula) and floor of the fourth ventricle in brains of the five cases examined. However, only in one of these was a yellow formaldehyde-induced fluorescence observed (on the fourth ventricle floor). Its discrete granular appearance, rapid fading and colour were typical of supra-ependymal 5-HT nerve fibres observed in rat brain. Very recent investigations on serial cryostat sections of rat brain ventricle regions revealed the absence of an immunohistochemical reaction with antisera to substance P, leu- and met-enkephalin and glutamic acid decarboxylase, but the presence of a reaction with 5-HT antiserum. The target for impulse-released 5-HT from this nonsynaptic 5-HT nerve plexus, bathed in cerebrospinal fluid, is not yet known.
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PMID:Demonstration of supra-ependymal 5-HT nerve fibres in human brain and their immunohistochemical identification in rat brain. 702 69

This study investigated the cholinesterasic reactivity of catecholamine neurons in the rat hindbrain with the aid of a two-step histochemical procedure. First, catecholamine cells were visualized by their formaldehyde/glutaraldehyde induced specific histofluorescence and then poststained in the same tissue with a thiocholine technique for acetylcholinesterase (AChE). Processing the vibratome-sectioned tissue in phosphate buffer subsequent to initial aldehyde fixation permitted satisfactory preservation of both amine fluorophores and esterasic reactivity. Our results, in both randomly sampled and serially sectioned material, unequivocally establish the presence of AChE in all pontomedullary cell groups emitting catecholamine fluorescence, the majority of which are known to consist of noradrenaline perikarya. Hence in contrast to previous reports the occurrence of AChE in central noradrenaline neurons appears to be generalized. The intensity of histofluorescence and esterasic staining were uncorrelated in most regions. It remains for future study to determine whether AChE in brain catecholamine neurons indicates their cholinoceptivity or subserves the catabolism of other neuromediators such as substance P.
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PMID:Acetylcholinesterase in pontomedullary catecholamine neurons of the adult albino rat. 706 9

The aim of the present investigation was to study the developing peptidergic innervation of the human fetal heart of 7-24 wk gestational age. An immunohistochemical approach was adopted and the total innervation visualised with antisera to general neuronal and Schwann cell markers, while the onset and development of specific neuropeptide-containing subpopulations were investigated using antisera to neuropeptide Y (NPY), somatostatin, vasoactive intestinal polypeptide (VIP), calcitonin gene-related peptide (CGRP) and substance P (SP). Cardiac ganglia and nerves were demonstrated from 7 wk of gestation whereas peptide-immunoreactive nerves were not observed until the 10th week of gestation. NPY-immunoreactive nerve fibres constituted the major subpopulation of peptide-containing nerves identified in the fetal heart, exhibiting a descending atrial to ventricular density gradient, and were first identified during the 10th wk of gestation. Somatostatin- and VIP-immunoreactive nerves appeared at 10-12 wk of gestation and were mainly distributed in the atria. Somatostatin immunoreactivity was localised to cell bodies in cardiac ganglia, as well as to nerve fibres, indicating an intrinsic origin for this nerve subpopulation. Conversely, the other peptide-containing nerves appear to be of extrinsic origin, including those immunoreactive for VIP. Intracardiac neurons exhibit a transient expression of tyrosine hydroxylase immunoreactivity. Putative sympathetic nerve fibres, displaying tyrosine hydroxylase and NPY immunoreactivity, were demonstrated before the adrenergic innervation has previously been shown to be present by formaldehyde-induced fluorescence staining of catecholamines. The onset of the CGRP- and SP-immunoreactive innervation, at 18-24 wk of gestation, followed the appearance of other peptide-containing nerves, suggesting that the sensory, afferent innervation occurs later than the autonomic. The differential appearance and distribution of peptide-containing nerve subpopulations indicate that there is a chronological order to the development of the autonomic and sensory components of human cardiac innervation.
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PMID:Development of the peptidergic innervation of human heart. 750 78

Serial sections of bone and soft tissue from the metacarpophalangeal joints of 2 mature and 2 immature horses were evaluated for substance P immunoreactive sensory nerve fibers. Formalin-fixed specimens were sectioned, either nondemineralized or demineralized with formic acid or EDTA. Rabbit antiserum to substance P (SP) was used in the streptavidin-biotin-peroxidase complex method for immunolocalization of SP antigen, and staining with 3,3'-diaminobenzidine was used for permanent identification of SP fibers. Abundant sensory nerve fibers were identified in the joint capsule, synovial membrane subintimal layers, collateral ligaments, suspensory ligament and distal sesamoidean ligament attachments to the sesamoid bones, and the periarticular periosteal layers. Sparse SP-immunoreactive nerve fibers were found in subchondral bone plates of the metacarpus, proximal first phalanx, and dorsal articular surface of the sesamoid bones. Most SP fibers were associated with blood vessels in the small cancellous spaces and haversian canals of the subchondral bone. The deeper marrow spaces contained increased numbers of SP sensory fibers; a few appeared in small groups and as several SP-immunoreactive fibers in a larger nerve. Cortical bone contained only a few SP fibers in the haversian canals. Substance P fibers were not identified in the osteocytic lacunae, canaliculi, or the bony lamellae of the haversian systems of the subchondral bone plate, and its extension to the metaphyseal and diaphyseal cortical bone. Equine metacarpophalangeal joint soft tissues have an abundant sensory nerve supply, similar to that of other species.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Substance P immunohistochemical study of the sensory innervation of normal subchondral bone in the equine metacarpophalangeal joint. 751 59

The contribution of the intracellular messengers nitric oxide, arachidonic acid and protein kinase C to persistent nociception in response to tissue injury in rats was examined following the subcutaneous injection of formalin into the hindpaw. Formalin injury-induced nociceptive behaviours were reduced by intrathecal pretreatment with inhibitors of nitric oxide synthase (NG-nitro-L-arginine methyl ester, L-NAME), arachidonic acid (dexamethasone) or protein kinase C [protein kinase C (19-26) and 1-95-(isoquinolinesulphonyl)-2-methylpiperazine dihydrochloride, H-7]. Each of these agents affected the tonic, but not the acute, phase of the formalin response. Furthermore, none of these agents affected mechanical or thermal flexion reflex thresholds in rats not injected with formalin. Conversely, formalin-induced nociceptive responses were enhanced by stimulators of nitric oxide (sodium nitroprusside), arachidonic acid metabolism (arachidonic acid) or protein kinase C [(+/-)-1-oleoyl-2-acetyl-glycerol], and were slightly reduced by inositol trisphosphate. Mechanical flexion reflexes were also reduced by arachidonic acid, while thermal flexion reflexes were reduced after treatment with sodium nitroprusside, arachidonic acid or [(+/-)-1-oleoyl-2-acetyl-glycerol]. The enhancement of formalin nociceptive behaviours (hyperalgesia) in rats treated with L-glutamate or substance P was reversed by pretreatment with inhibitors of nitric oxide (L-NAME), arachidonic acid (dexamethasone) or protein kinase C (H-7). The results suggest that central sensitization and persistent nociception following formalin-induced tissue injury, and the hyperalgesia in the formalin test induced by L-glutamate and substance P, are dependent on the intracellular messengers nitric oxide, arachidonic acid and protein kinase C.
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PMID:Intracellular messengers contributing to persistent nociception and hyperalgesia induced by L-glutamate and substance P in the rat formalin pain model. 752 41

Homogenates of chick dorsal root ganglia (DRG) and in vitro cultures of DRG neurons are known to synthesize prostaglandin (PG) D2. To specify the PGD synthase isozymes controlling PGD2 synthesis in DRG and to identify the DRG cells responsible for this synthesis, we applied polyclonal antibodies raised against rat brain or rat spleen PGD synthase isozymes to vibratome or cryostat slices of DRG previously fixed with a formaldehyde-lysine-periodate mixture and permeabilized with Triton X-100. The immunoreactivity indicating rat spleen PGD synthase, a glutathione (GSH)-requiring enzyme, was located in satellite cells encompassing particular large neurons of class A and in Schwann cells myelinating and enwrapping their initial axonal segments. In contrast, the immunoreactivity of rat brain PGD synthase, a GSH-independent enzyme, was restricted to particular ganglion cell perikarya: 33% of the DRG neurons were immunostained for rat brain PGD synthase, including 2% of large class A neurons and 40% of small class B neurons. Only 3.3% of rat brain PGD synthase-immunoreactive small B neurons coexpressed substance P, indicating that the immunoreactive neurons belong to the B1 subclass. By electron microscopy, 71 of 72 immunoreactive DRG cells were identified as small B neurons of the B1 subclass, and 71 of 77 B1 neurons were immunoreactive for rat brain PGD synthase. These results demonstrate that PGD2 formation in DRG is regulated by two isozymes: the GSH-requiring isozyme located in satellite and Schwann cells and the GSH-independent isozyme-confined to small B1 neurons.
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PMID:Neuronal and glial prostaglandin D synthase isozymes in chick dorsal root ganglia: a light and electron microscopic immunocytochemical study. 752 29

We compared the behavioral effects of treatment with pruritogenic and algesiogenic agents in mice. The animals were given subcutaneous injections of pruritogenic agents, compound 48/80 (3-100 micrograms), substance P (10-300 micrograms) and histamine (3-300 micrograms), and algesiogenic agents, capsaicin (30 and 100 micrograms) and dilute formalin (5 mg of formaldehyde), into the rostral back, and scratching of the injected site by the hind paws was counted. Compound 48/80 and substance P dose dependently elicited the scratching behavior, but histamine, capsaicin and dilute formalin were without significant effects at the doses examined. These results suggest that compound 48/80- and substance P-induced scratching of the injected site is due to itch, but not to pain. The data did not provide support for the idea that histamine produces itch in the mouse.
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PMID:Scratching behavior induced by pruritogenic but not algesiogenic agents in mice. 753 79

Swelling, oedema, and loss of fluids and protein from the vascular compartment are immediate responses seen in living tissues after severe injury. Peptides of the corticotropin-releasing factor (CRF) superfamily have the unusual property of preventing the vascular leakage that occurs in tissues after damage. For example, CRF decreased protein extravasation, oedema and swelling in the anaesthetized rat's paw after exposure to heat or to extreme cold, in tracheal mucosa after exposure to formaldehyde, in skeletal muscle after a knife cut, and in brain cortex after freezing. The anti-inflammatory actions of CRF were independent of steroid release or hypotensive effects. CRF was a functional antagonist of inflammatory mediators such as histamine and substance P. It inhibited neurogenic inflammation, but interactions with unmyelinated sensory neurons did not account for the wide range of CRF's anti-inflammatory activities. Localized application of CRF prevented histamine-induced leaks in the hamster cheek pouch, and displaceable binding sites to iodinated CRF were found on blood vessels and on epithelial cells in close proximity to sites of vascular leakage. These results indicated peripheral sites of action. CRF may be the first example of a peptide hormone demonstrated to have potent anti-inflammatory agonist actions in vivo.
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PMID:Peripheral anti-inflammatory actions of corticotropin-releasing factor. 768 82

Dental injuries have been shown to generate extensive structural and cytochemical changes in sensory fibers that contain neuropeptides such as calcitonin gene-related peptide (CGRP) or substance P (SP). The present study was designed to test whether the anti-inflammatory drug dexamethasone (DEX) can alter neural responses to dental injuries. DEX (20 micrograms/100 g body weight) was given to adult rats (n = 10) prior to dental surgery and daily thereafter for 4 days. Control animals received sterile saline vehicle (n = 6) or no injection (n = 1). Each rat was then anesthetized for dental surgery and a cavity was drilled partway through dentin on the anterior side of the right maxillary first molar. Pulp exposure injuries were also made on two right mandibular molars in 14 of 17 rats. After 4 days of daily drug treatment, the rats were anesthetized and fixed by perfusion with formaldehyde-picric acid, and their jaws were prepared for immunocytochemistry. Neural CGRP immunoreactivity near the maxillary cavity injury site of DEX-treated rats was reduced more than 50% compared to controls, as determined both qualitatively and by digital analysis. The SP immunoreactive (IR) fibers in molar pulp also had extensive inhibition of neural reactions to cavity injury. DEX also reduced the immunoreactivity for CGRP and SP in normal contralateral rat molars of all treated rats, and it caused a postoperative loss of weight. Pretreatment for 1-5 days prior to the 4 day injury gave the same results as pretreatment for 1 h. The mandibular pulp exposure injuries induced a chronic abscess and advancing pulpal necrosis but did not show differences in nerve reactions between DEX-treated rats and the controls. In conclusion, the synthetic steroid dexamethasone suppressed the CGRP and SP neuropeptide immunoreactivity in normal dental nerves and it reduced nerve-sprouting responses to dentin cavity injuries; however, sensory nerve reactions to pulpal exposure injuries were not affected by DEX in these experiments.
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PMID:Dexamethasone treatment reduces sensory neuropeptides and nerve sprouting reactions in injured teeth. 790 26


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