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 neuro-endocrine cells of fish skin and respiratory surfaces, and their bioactive secretion as far as is known, are reviewed, and compared with similar elements in tetrapods, particularly amphibians. In the skin of teleost fish, immunohistochemistry has shown that Merkel cells react for serotonin, neuron-specific enolase and enkephalins. The pharmacology is not established in dipnoans or lampreys. In some teleosts, neuromasts react for substance P and leu-enkephalins; substance P is also reported from some ampullary organs (electroreceptors). Taste buds of teleosts may react for enkephalin and substance P. Basal cells of taste buds react for serotonin and neuron-specific enolase. Some unicellular skin glands of teleosts express bioactive compounds, including serotonin and some peptides; this ectopic expression is paralleled in amphibian skin glands. The dipnoan Protopterus has innervated pulmonary neuro-endocrine cells in the pneumatic duct region with dense-cored vesicles. In Polypterus and Amia the lungs have serotonin-positive neuro-endocrine cells that are apparently not innervated. In fish gills, a closed type of neuro-endocrine cell reacts for serotonin, an open type for enkephalins and some calcium-binding proteins (calbindin, calmodulin and S-100 protein). The functions of neuro-endocrine cells in fishes await investigation, but it is assumed they are regulatory.
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PMID:Distribution patterns of the paraneuronal endocrine cells in the skin, gills and the airways of fishes as determined by immunohistochemical and histological methods. 798 86

Substance P receptor-expressing neurons in the rat cerebral neocortex were examined by single- and double-immunolabeling methods with an affinity-purified specific antibody to substance P receptor. Substance P receptor immunoreactivity was observed exclusively in non-pyramidal neurons. About a quarter of these substance P receptor-positive neocortical neurons showed intense immunoreactivity, and the other three quarters displayed weak substance P receptor immunoreactivity. The neurons showing intense substance P receptor immunoreactivity were large multipolar cells with a few long aspiny or sparsely-spiny dendrites, and were scattered throughout the neocortical layers except for layer I, and also in the underlying white matter. The weakly immunoreactive neurons were medium-sized multipolar cells with oval to round somata and aspiny varicose dendrites, and were distributed in all cortical layers with a bias to layers II-III and the superficial part of layer V. The double-immunofluorescence study revealed that almost all substance P receptor-positive neurons were immunoreactive for GABA, but negative for glutaminase. Substance P receptor immunoreactivity in GABAergic neocortical neurons were further examined by the double-immunofluorescence method with antibodies to markers for subgroups of GABAergic neurons. Somatostatin immunoreactivity was found in 89% of neurons with intense substance P receptor immunoreactivity, and in 1.5% of neurons with weak substance P receptor immunoreactivity. Neuropeptide Y immunoreactivity was also observed in 92% of neurons with intense immunoreactivity for substance P receptor, and in 1.6% of neurons with weak immunoreactivity for substance P receptor. In contrast, parvalbumin immunoreactivity was seen in 1.3% of neurons with intense substance P receptor immunoreactivity, and in 59% of weak substance P receptor immunoreactivity. Calbindin D28k immunoreactivity was found in 12 and 19% of neurons, respectively, with weak and intense immunoreactivities for substance P receptor. Virtually no cells showing substance P receptor immunoreactivity displayed immunoreactivity for vasoactive intestinal polypeptide or choline acetyltransferase. These results indicate that the neocortical neurons expressing substance P receptor constitute a subpopulation of GABAergic non-pyramidal cells, and are segregated into neurons with intense immunoreactivity and those with weak immunoreactivity for substance P receptor; the vast majority of neurons with intense substance P receptor immunoreactivity contain somatostatin and neuropeptide Y, and the majority of neurons with weak substance P receptor immunoreactivity have parvalbumin.
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PMID:Morphological and chemical characteristics of substance P receptor-immunoreactive neurons in the rat neocortex. 805 13

The efferent connections of the rostral pole of the rat accumbens, where distinct core and shell subterritories can not be identified, were examined with the aid of the anterogradely transported plant lectin, Phaseolus vulgaris-leucoagglutinin (PHA-L), for comparison with the previously reported projection patterns of the accumbal core and shell. Injection sites and transported PHA-L were evaluated with the aid of reference to adjacent sections processed to display substance P or calbindin 28 kD immunoreactivities, i.e., markers that demonstrate the core and shell. Lateral parts of the rostral pole gave rise to a "core-like" projection system that involved the rostroventral globus pallidus, subcommissural ventral pallidum, entopeduncular nucleus and an adjacent part of the lateral hypothalamus, lateral ventral tegmental area, dorsal pars compacta, and structures in the lateral mesencephalic tegmentum and central grey. The medial part of the rostral pole gave rise to a "shell-like" innervation of the subcommissural ventral pallidum, lateral preoptic region, lateral hypothalamus, ventral tegmental area, dorsalmost pars compacta, retrorubral field, lateral midbrain tegmentum, and central grey. In contrast to the large numbers of axon varicosities observed through the entire length of lateral hypothalamus following shell injections, dense accumulations of axon collaterals and varicosities in hypothalamus were limited to the levels of origin of the stria medullaris bundle and entopeduncular nucleus and to the posterlateral region following medial injections. The medial part of the rostral pole contributed some projections to preoptic and sublenticular regions, but not to the bed nucleus of the stria terminalis. Noteworthy concentrations of calbindin immunoreactive cells observed in the lateral rostral pole correlate with the origin of the "basal ganglia-like" projection system, provoking the speculation that ventral striatal calbindin immunoreactive cells contribute principally to basal ganglia-like projections while cells lacking calbindin immunoreactivity contribute to the innervation of hypothalamus and midbrain tegmentum.
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PMID:Specificity in the efferent projections of the nucleus accumbens in the rat: comparison of the rostral pole projection patterns with those of the core and shell. 842 43

Excitotoxin lesions induced by quinolinic acid (QA) were made unilaterally in the caudate nucleus and putamen of 12 rhesus monkeys. Both acute (2-3 weeks) and chronic (4-6 months) effects were evaluated. Excitotoxin striatal lesions were characterized by a central zone of intense astrogliosis and marked neuronal depletion, which was surrounded by a transition zone in which there was partial neuronal sparing throughout the entire lesioned side. Immunocytochemical and enzyme histochemical markers for both large and medium-sized aspiny- and spiny-striatal neurons clearly demonstrated a selective pattern of neuronal vulnerability to the excitotoxic effects of QA within lesioned striata. Medium-sized spiny neurons containing calbindin Dk28, enkephalin, and substance P were disproportionately lost, while aspiny neuronal subpopulations containing NADPH diaphorase (NADPH-d) and choline acetyltransferase activity (ChAT) were relatively spared. Combined labeling by NADPH-d enzyme histochemistry and Nissl staining, as well as NADPH-d histochemistry and calbindin Dk28 immunocytochemistry, demonstrated significant increases in the ratio of aspiny to spiny neurons within the lesioned striata. Neurochemical measurements confirmed a loss of GABA and substance P-like immunoreactivity yet no significant depletion of somatostatin-like immunoreactivity, neuropeptide Y-like immunoreactivity, or ChAT were seen. The striatal patch-matrix pattern persisted, as demonstrated by acetylcholinesterase activity. The pattern was altered, however, in the chronic animals, such that the matrix zone was significantly reduced, while the total area of patches remained within normal limits. Ultrastructural analysis confirmed axon sparing lesions with neuronal loss and astrogliosis. Pretreatment of 3 monkeys with MK-801, a noncompetitive N-methyl-D-aspartate (NMDA) antagonist, blocked striatal QA neurotoxicity. The present results provide an experimental primate model which closely resembles the neuropathologic and neurochemical features of Huntington's disease. These findings further strengthen the possibility that an NMDA receptor-mediated excitotoxic process plays a role in the pathogenesis of this disorder.
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PMID:Excitotoxin lesions in primates as a model for Huntington's disease: histopathologic and neurochemical characterization. 843 51

A number of marker substances for neuronal and neuroendocrine cells have been demonstrated in the cytoplasm of the interstitial Leydig cells of human testes using basic immunocytochemical methods and some of their modifications. We were able to reveal immunoreactivity for enzymes involved in the synthesis of the catecholamines dopamine and noradrenaline (tyrosine hydroxylase, aromatic L-amino acid decarboxylase, dopamine-beta-hydroxylase), for the indolamine 5-hydroxytryptamine (serotonin), as well as for a number of well-known neuronal markers such as the neurofilament protein 200, synaptophysin, chromogranin A + B, the neural cell-adhesion molecule (N-CAM), the microtubule-associated protein (MAP-2), and the calcium-binding proteins: S-100, calbindin and parvalbumin. Immunoreactivity for these substances was found in the majority of the interstitial cells although differences in the staining intensity among the individual Leydig cells and among Leydig cells from different patients were observed. At the electron-microscopic level the Leydig cell cytoplasm was seen to contain microtubules, intermediate- and microfilaments as well as clear (40-60 nm) and dense-core (100-300 nm) vesicles, providing a morphological correlate for some of the immunocytochemical results. Although individual marker substances are not absolutely specific for nerve and neuroendocrine cells, the results obtained, together with the already established neuron-specific enolase-, substance P-, methionine-enkephalin- and proopiomelanocortin (POMC)-derived peptide-like immunoreactivity, provide strong evidence for the neuroendocrine (paraneuronal, APUD-like) nature of the Leydig cells of the human testis.
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PMID:The Leydig cell of the human testis--a new member of the diffuse neuroendocrine system. 847 1

The distribution of laryngeal taste buds (TBs) and their neutral components in the cat were investigated by immunohistochemistry and electron microscopy. The antisera used in this study were against cytokeratin, protein gene product 9.5 (PGP9.5), neuron-specific enolase (NSE), S-100 protein, calbindin D, calcitonin gene-related peptide (CGRP), and substance P (SP). Taste bud cells were specifically immunoreactive to the antibodies of human cytokeratin subtypes 8 and 18 (CAM5.2). On observation with CAM5.2, TBs were seen distributed on the laryngeal surface of the epiglottis and spread caudally along the aryepiglottic folds, reaching peak density at the laryngeal side of the arytenoid tubercle. The PGP9.5 and NSE immunoreactivities were recognized in TB cells and nerve fibers, both within the TBs and in the subepithelial connective tissue. S-100 protein immunoreactivities were not found in any of the cells in the TBs but were found exclusively in the subepithelial neural elements. The calbindin-D, CGRP, and SP immunoreactivities were confined to a part of the neural elements that was very thin. Taste pores, taste villi, neuronal varicosity, and synapselike structures were observed by scanning and transmission electron microscopic study. From these results it is considered that the TBs act as a chemical receptor.
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PMID:Morphologic study of the laryngeal taste buds in the cat. 852 84

Preferential loss of basal ganglia neurons and terminals occurs in Huntington's disease (HD). Terminals of preproenkephalin medium-size spiny neurons are more vulnerable than terminals of preprotachykinin neurons, but the peptidergic neurons of origin have not yet been shown to die preferentially. We sought to determine, in the striatum, whether preproenkephalin neurons were lost to a greater extent than preprotachykinin neurons and to determine whether there were decreases in specific messenger RNA (mRNA) levels of preproenkephalin, preprotachykinin, and calbindin D28k. We found a grade-related decrease in the number of preprotachykinin- and calbindin D28k-labeled neurons per measuring field in the caudate nucleus of patients with HD. Three measures of the neuronal level of preprotachykinin mRNA were all significantly reduced (6-65% of control values) in HD caudate nucleus. No decline in calbindin D28k mRNA levels per neuron were found in HD striata compared to control striata. We found a greater loss of preproenkephalin neurons per field than preprotachyknin neurons per field in the caudate nucleus of HD brains compared to control brains. Preprotachykinin neurons are lost in HD in a grade-related manner and surviving preprotachykinin neurons are impaired in function. However, preproenkephalin neurons are lost to a greater extent than preprotachykinin neurons, which may explain preferential changes found in projection regions of the striatum. Declines in neuropeptide mRNA may be specific in HD, since calbindin D28k mRNA levels were unchanged. Alterations in the levels of expression of preproenkephalin and preprotachykinin mRNA may be direct or indirect effects of the HD mutation.
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PMID:Preferential loss of preproenkephalin versus preprotachykinin neurons from the striatum of Huntington's disease patients. 852 54

The antimitotic drug methylazoxymethanol was used to destroy striatal patch neurons during their three-day-period of neurogenesis in the rat. Single or multiple injections of methylazoxymethanol were given during embryonic days 13-15, the period when patch neurons are known to undergo their final cell division. Methylazoxymethanol treatments produced a dramatic reduction in striatal volume. Immunocytochemical analysis revealed the continued presence of patches of neurons that were substance P-immunoreactive and devoid of calbindin and enkephalin immunoreactivity. Both the number of patches and relative volume occupied by patches was reduced in methylazoxymethanol-treated striata. Patch neurons could also be labelled by an intrastriatal injection of FluoroGold during the first postnatal week. The early ingrowth of nigrostriatal dopamine afferents was less noticeably patchy in the methylazoxymethanol-treated animals, in part owing to an overall increase in density. Large reductions in the number of neurons immunoreactive for choline acetyltransferase were observed, whereas NADPH diaphorase-stained neurons were not reduced unless methylazoxymethanol was given on embryonic day 15. Injections of bromo-deoxy-uridine, either during or after the 24 h that each methylazoxymethanol injection was considered to be effective, revealed that (i) some patch neurons continued to be generated in the 24-h period following methylazoxymethanol administration, and (ii) many patch neurons were generated after the effects of methylazoxymethanol had worn off. These findings demonstrate that it was impossible to completely eliminate the patches using methylazoxymethanol injections during the period of patch neurogenesis. However, methylazoxymethanol treatment during this time did produce a dramatic loss of cells and a relatively greater reduction in patch volume. Despite this disruption, the appropriate compartmentalization of neuroactive substances appeared to be maintained.
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PMID:The development of striatal patch/matrix organization after prenatal methylazoxymethanol: a combined immunocytochemical and bromo-deoxy-uridine birthdating study. 857 71

Immunohistochemical techniques were used to examine the presence and co-localisation of a range of putative neurotransmitters and other neuronal markers in the myenteric plexus of the small and large intestine of the mouse. Distinct sub-populations of myenteric neurons were identified, based on the combinations of substances they contained and the distribution of their fibres. In the small intestine, there were two major classes of circular muscle motor neurons; one class was characterised by the presence of nitric oxide synthase, vasoactive intestinal peptide plus neuropeptide Y (NOS/VIP/NPY), and the second class contained calretinin plus substance P (CalR/SP). There were seven classes of neurons that innervated myenteric ganglia; these contained nos, vip, nos/vip, npy, calr/calbindin (calb), sp or 5-ht. In the large intestine, there were five major classes of motor neurons that contained nos, nos/vip, gaba, sp, or calr/sp, and seven major classes of neurons that innervated myenteric ganglia and contained nos, vip, calr/calb, calr, sp, gaba or 5-ht. Although some aspects of the patterns of co-localisation are similar to those in other species, this study re-inforces recent analyses that indicate significant species differences in neurochemical patterns in the enteric neurons of different species.
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PMID:Chemical coding of neurons in the myenteric plexus and external muscle of the small and large intestine of the mouse. 860 Dec 95

The present study compares the distribution of three calcium binding proteins, calbindin-D28k, calretinin, and parvalbumin, in the midbrain tegmentum of rats and humans. In order to compare the distributions of these proteins directly, the cytoarchitecture of this region was evaluated by using immunohistochemistry for tyrosine hydroxylase and substance P in serial sections in both transverse and horizontal planes. There was a high degree of homology in the cytoarchitecture of the three main dopaminergic regions identified. The A8 group was localised in the retrorubral fields, which extended rostrally into the midbrain reticular fields in the human. The A9 group corresponded to the substantia nigra, which was delimited by its dense substance P innervation. The heterogeneous A10 group, situated along the dorsal border as well as medial to the A9 group, comprised multiple nuclei. The distribution of calcium binding proteins was similar in both species, although a larger proportion of neurons contained these proteins in the rat. Calbindin-D28k was localised in neurons within A8 and A10 nuclei and within the caudomedial A9 region (and rostrolateral A9 in the rat only). Calretinin was localised in similar regions. In contrast, neurons containing parvalbumin were concentrated in the substantia nigra pars reticulata. The results suggest that few dopaminergic neurons receiving striatal input in the substantia nigra contain calcium binding proteins; rather, the nondopaminergic nigral neurons contain parvalbumin. Interestingly, dopaminergic neurons are more numerous in humans, whereas nondopaminergic neurons predominate in rats, which suggests that functional differences may exist between rats and humans.
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PMID:Cytoarchitectural distribution of calcium binding proteins in midbrain dopaminergic regions of rats and humans. 878 81


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