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)

In order to further investigate the neurochemical anatomy of the primate nucleus accumbens (NAC), the distributions of the neuropeptides leucine-enkephalin (Leu-ENK), neurotensin (NT), and substance P (SP) and of haloperidol-induced c-fos expression were investigated in the macaque monkey using immunohistochemical methods. To define the boundaries of the NAC, dopamine (DA) and tyrosine hydroxylase (TH) immunohistochemistry was performed. In addition, to formulate the distinction between subdivisions of the nucleus accumbens, immunohistochemistry for calbindin-D28 (CBD) and SP was employed. In general, the medial part of NAC, which consisted of small to medium-sized cells, was low for CBD immunoreactivity and moderate to high for SP immunoreactivities, while the dorsolateral part, which was composed of small cells, showed the opposite pattern of immunostaining for CBD and SP. Many Leu-ENK-immunoreactive perikarya were observed in the dorsal NAC at its middle and caudal levels. There were moderate densities of Leu-ENK-positive fibers throughout the medial part of the NAC. At the dorsolateral margin of the NAC, Leu-ENK-positive fibers formed patches. Most NT-positive perikarya were found in the dorsolateral subdivision. SP-positive perikarya were scarce in the NAC. Dense distribution of NT- and SP-containing fibers or puncta were observed in the mediodorsal part (medial subdivision), where a dense field of DA-immunoreactive fibers was observed. The ventral part (ventral subdivision) contained moderate numbers of NT- and SP-immunoreactive fibers. Haloperidol-induced c-fos expression was very extensive in the medial half of NAC, particularly in the mediodorsal region, which overlapped with the DA- and peptide-rich region. The present study indicates that the NAC of the primate can be subdivided into at least three subterritories, the dorsolateral, medial and ventral subdivision, by neuropeptide histochemistry as well as by the response of its constituent neurons to haloperidol.
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PMID:Neurochemical heterogeneity of the primate nucleus accumbens. 754 84

Repeated episodes of cerebral hypoxia-ischemia can cause primarily striatal neuronal loss in the developing brain. We investigated the effect of repeated episodes of asphyxia on specific neuronal sub-populations of the basal ganglia in late-gestation fetal sheep. Asphyxia was induced in 10 fetal sheep (118-126 days gestation) by occluding the umbilical cord for 5 min. This procedure was repeated four times at 30 min intervals and the brains were fixed 3 days later for histopathology. Immunohistochemical markers were used to identify various populations of neurons in the striatum. Antibodies to calbindin were used to stain the GABAergic medium-sized striatal projection neurons and antibodies to somatostatin and parvalbumin to identify striatal interneurons. Striatal projection neurons to the globus pallidus were recognized by enkephalin immunoreactivity, while the striatonigral terminals were identified in the substantia nigra pars reticulata by substance P immunohistochemical labelling. The results showed a marked loss of calbindin staining in the striatum, evident by both reduced cell numbers and a decrease in neuropil staining. The number of parvalbumin immunoreactive cells was also reduced in the striatum, while somatostatin interneurons were selectively preserved. In addition, immunostaining for enkephalin in the globus pallidus and for substance P in the substantia nigra was markedly reduced. These results show that the stiatal GABAergic medium-sized projection neurons are severely affected by recurrent episodes of asphyxia. These findings are confirmed and extended by the results demonstrating that both the enkephalin/GABA striatopallidal and the substance P/GABA stiatonigral pathways are affected. The results of this study therefore suggest that the efferent striatal projections to the globus pallidus and to the substantia nigra may be involved in asphyxial episodes resulting in cerebral palsy.
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PMID:Repeated asphyxia causes loss of striatal projection neurons in the fetal sheep brain. 760 81

The effect of prenatal cocaine on the anatomical development of the striatum was examined. The distribution and density of dopaminergic innervation of the striatum of animals exposed to cocaine during the second and third week of gestation was not noticeably different from prenatally saline-injected or untreated controls at any age. The patch/matrix organization of the striatum also appeared unaltered: neurons exhibiting dense substance P staining were localized to patches that overlapped dopamine terminal patches early in development, and enkephalin- and calbindin-immunoreactive neurons were found segregated to the matrix. Histochemical staining for acetylcholinesterase and NADPH diaphorase also revealed no differences between prenatally cocaine-treated and control brains. Whereas prenatal cocaine treatment failed to modify the basic compartmental organization of the striatum, it did lead to a hyperinnervation of serotonin-immunoreactive fibers which developed slowly after birth. Thus prenatal exposure to cocaine is capable of altering the ingrowth of serotonergic projections to the striatum while producing no change in the organization of neurons intrinsic to the striatum.
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PMID:Prenatal cocaine increases striatal serotonin innervation without altering the patch/matrix organization of intrinsic cell types. 769 34

The peripheral projections of two distinct subpopulations of primary sensory neurons, expressing either calbindin D-28k or substance P, were studied in chick hindlimbs by immunodetecting calbindin D-28k with a rabbit antiserum and substance P with a mouse monoclonal antibody. Calbindin D-28k-immunoreactive axons provided an innervation restricted to specific mechanoreceptors such as muscle spindles, Herbst and Merkel corpuscles, or collars of feather follicles but were absent from Golgi tendon organs. In contrast, substance P-positive axons spread out diffusely in muscles and skin, formed loose plexuses, and extended free branches to the endomysium, arteries, superficial dermis, or dermal pulp of feather follicles. The present results show that calbindin D-28k- and substance P-immunoreactive primary sensory neurons provide distinct modes of innervation to selective targets in peripheral tissues. The results suggest a possible correlation between CaBP-expressing nerve endings and rapidly adapting mechanoreceptors.
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PMID:Calbindin D-28k- and substance P-immunoreactive primary sensory neurons: peripheral projections in chick hindlimbs. 769

An impairment of energy metabolism may underlie slow excitotoxic neuronal death in neurodegenerative diseases. We therefore examined the effects of intrastriatal, subacute systemic, or chronic systemic administration of the mitochondrial toxin 3-nitropropionic acid (3-NP) in rats. Following intrastriatal injection 3-NP produced dose-dependent striatal lesions. Neurochemical and histologic evaluation showed that markers of both spiny projection neurons (GABA, substance P, calbindin) and aspiny interneurons (somatostatin, neuropeptide Y, NADPH-diaphorase) were equally affected. Subacute systemic administration of 3-NP produced age-dependent bilateral striatal lesions with a similar neurochemical profile. However, in contrast to the intrastriatal injections, striatal dopaminergic afferent projections were spared. Both freeze-clamp measurements and chemical shift magnetic resonance spectroscopy showed that 3-NP impairs energy metabolism in the striatum in vivo. Microdialysis showed no increase in extracellular glutamate concentrations after systemic administration of 3-NP. The lesions produced by intrastriatal injection or systemic administration of 3-NP were blocked by prior decortication. However, the NMDA antagonist MK-801 did not block the effects of intrastriatal 3-NP, consistent with a non-NMDA excitotoxic mechanism. In contrast to subacute systemic administration of 3-NP, chronic (1 month) administration produced lesions confined to the striatum in which there was relative sparing of NADPH-diaphorase interneurons, consistent with an NMDA excitotoxic process. Chronic administration showed growth-related proliferative changes in dendrites of spiny neurons similar to changes in Huntington's disease (HD). These results are consistent with in vitro studies showing that mild metabolic compromise can selectively activate NMDA receptors while more severe compromise activates both NMDA and non-NMDA receptors. Chronic administration of 3-NP over 1 month produces selective striatal lesions that replicate many of the characteristic histologic and neurochemical features of HD.
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PMID:Neurochemical and histologic characterization of striatal excitotoxic lesions produced by the mitochondrial toxin 3-nitropropionic acid. 769 9

Substance P immunoreactivity is localized in discrete subsets of neurons in the human cerebral cortex and basal ganglia. In the normal human cerebral cortex, a subset of aspiny local circuit neurons in deep cortical layers and the cortical subplate contain preprotachykinin mRNA and substance P immunoreactive. These neurons, which contain NADPH diaphorase (NO synthase) activity, are strikingly depleted in Alzheimer's disease--in contrast to other local circuit neurons--suggesting that they may be an early target of the degenerative process. In the human basal ganglia, substance P immunoreactivity and mRNA are localized in a subset of spiny striatal neurons that project to the internal segment of the globus pallidus. These neurons are enriched in D1 dopamine receptors and dynorphin, and are calbindin and DARP 32 immunoreactive. A separate subset of aspiny striatal local circuit neurons also contain substance P immunoreactivity. Fiber and terminal staining is prominent in the matrix compartment of the ventromedial striatum and persists dorsally as a rim outlining patches that contain lesser amounts of immunoreactivity. Intense fiber and terminal staining is found in the pars reticulata of the substantia nigra. In Huntington's disease, substance P is depleted in the striatum in parallel with the dorsoventral gradient of neuronal loss. Terminal staining is progressively depleted in the pallidum and substantia nigra in tandem with striatal atrophy. Substance P receptor immunoreactivity, defined with two polyclonal antisera raised against synthetic peptides derived from the substance P receptor sequence, intensely labels a subset of large neurons in the nucleus basalis and striatum identical to neurons labeled with choline acetyltransferase and nerve growth factor receptor antibodies (although striatal cholinergic neurons do not contain nerve growth factor receptor immunoreactivity in the human). These cholinergic neurons resist degeneration in Huntington's disease but are sensitive to degeneration in Alzheimer's disease. Less intensely labeled neurons include pyramidal neurons in the hippocampal CA2 field, nonpyramidal neurons in CA1-4, pyramidal and nonpyramidal neurons in deep neocortical layers and in the cortical subplate. Substance P receptor immunoreactivity is not well defined in the human globus pallidus or substantia nigra.
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PMID:Substance P and substance P receptor histochemistry in human neurodegenerative diseases. 769 86

Secretoneurin is a novel 33-amino-acid neuropeptide produced by endoproteolytic processing from secretogranin II, which is a member of the chromogranin/secretogranin family. In this immunocytochemical study, we compared the distribution pattern of secretoneurin immunoreactivity with that of tyrosine hydroxylase, calbindin, substance P, and Leu-enkephalin in adjacent sections of rat forebrain. Secretoneurin appeared mainly in varicosities and fibers. Only a few cell bodies were stained. In the nucleus accumbens, a partial overlap of secretoneurin-immunoreactive patches with enkephalin-immunopositive areas was found. Secretoneurin displayed low to moderate levels of immunoreaction in calbindin-rich as well as in calbindin-immunonegative areas of the caudate-putamen. In the globus pallidus, entopeduncular nucleus, and substantia nigra, secretoneurin immunoreactivity was oriented ventromedially preferentially in woolly fibers. The dense immunostaining in the medial nucleus accumbens was directly continuous with dense secretoneurin immunoreactivity in the bed nucleus of the stria terminalis. Two strongly secretoneurin-immunopositive bands, one in the sublenticular portion and a smaller one along the posterior limb of the anterior commissure, interconnected the highly secretoneurin-immunopositive centromedial amygdala with the bed nucleus of the stria terminalis. Thus, the distribution pattern of secretoneurin immunoreactivity provides a marker of the extended amygdala that forms a continuum between the centromedial amygdala and the bed nucleus of the stria terminalis.
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PMID:Evidence for a high density of secretoneurin-like immunoreactivity in the extended amygdala of the rat. 774 36

The goal of the present study was to identify cytochemical markers characteristic of muscle afferents in hatchling chicks. To this end, we stained neurons in the trigeminal mesencephalic nucleus with a variety of markers that label subsets of neurons in avian dorsal root ganglia. We found that trigeminal mesencephalic neurons are surprisingly heterogeneous in their cytochemical make-up, expressing, to varying degrees, substance P, cholecystokinin, carbonic anhydrase, calbindin D-28k, parvalbumin, and S-100 beta. Calbindin D28k and S-100 beta appeared to be expressed equally in medial and lateral divisions of the trigeminal mesencephalic nucleus. In contrast, substance P- and cholecystokinin-immunoreactive neurons were more abundant in the medial division, whereas carbonic anhydrase activity and parvalbumin immunoreactivity were stronger in the lateral division. We were unable to detect met-enkephalin, neuropeptide Y, calcitonin gene-related peptide, vasoactive intestinal peptide, somatostatin, gamma-aminobutyric acid, or tyrosine hydroxylase in the trigeminal mesencephalic nucleus. Moreover, these neurons did not appear to bind the lectin Dolichos biflorus agglutinin. The heterogeneity of expression of markers among trigeminal mesencephalic nucleus neurons, especially between neurons in the medial and lateral divisions, suggests that these neurons are functionally diverse.
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PMID:Cytochemical characteristics of neurons in the trigeminal mesencephalic nucleus of hatchling chicks. 788 44

Immunocytochemical properties of dorsal root ganglion neurons innervating the kidney were studied with retrograde tracing of Fluorogold or Fast Blue dyes applied to the cut renal nerves in the rat. The proportions and sizes of renal afferent neurons labelled with a variety of markers were quantified in T9-L1 dorsal root ganglia from five rats. Compared with the overall size distribution in these ganglia, renal afferent neurons were mainly small with a few medium-sized neurons. The majority (79%) of renal afferent dorsal root ganglion neuronal somata were unlabelled by an anti-neurofilament antibody, RT79, and classified as neurofilament-poor with probable C-fibres. These had an approximately normal distribution of cell sizes. Only 21% were RT79-positive and classified as neurofilament-rich with probable A-fibres, and even these were small to medium sized cells, consistent with them being mostly A delta-fibre neurons. Percentages of renal afferent neurons showing labelling were as follows: peripherin-like immunoreactivity: 69%; calcitonin-gene related peptide: 93%; substance P: 37%; the lectins soybean agglutinin: 57% and peanut agglutinin: 68%; Calbindin D28k-like immunoreactivity: 21% (only weak labelling); carbonic anhydrase like immunoreactivity: 0%. There were differences between probable C-fibre and probable A-fibre neurons, classified according to their labelling with RT97. The percentages of RT97-negative and RT97-positive neurons respectively labelled with the other markers were as follows: peripherin-like immunoreactivity: 82%, 25%; calcitonin gene-related peptide-like immunoreactivity: 99%, 79%; substance P-like immunoreactivity: 43%, 0%; soybean agglutinin: 69%, 24%; peanut agglutinin: 76%, 47%; calbindin-like immunoreactivity: 26%, 0%. Thus, the biggest differences between the probable A- and C-fibre renal afferent neurons were in their peripherin, substance P and calbindin contents. Thus, renal afferent neurons in the dorsal root ganglion are not homogeneous and it is suggested the differences may relate to the known different afferent receptor types within the kidney. It is suggested that the low proportion of neurons with substance P-like immunoreactivity in the renal afferent innervation compared to that of other viscera may relate to the role of the renal vasculature in urine formation.
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PMID:Immunocytochemical properties of rat renal afferent neurons in dorsal root ganglia: a quantitative study. 789 54

A number of neuroendocrine and neuronal markers were demonstrated in Leydig cells of the testes of 18 men aged between 20 and 81 years. Tissue sections were divided into five groups, i.e. carcinoma of the prostate (control cases; n = 4), seminoma (n = 8), anti-androgen therapy (n = 3), oestradiol therapy (n = 2) and cryptorchidism (n = 1). The following substances were immunocytochemically tested: the monoamine synthesizing enzymes tyrosine hydroxylase, aromatic L-amino acid decarboxylase, dopamine-beta-hydroxylase and phenylethanolamine-N-methyltransferase, the indolamine serotonin, the calcium-binding proteins parvalbumin, calbindin and S-100 protein, the microtubule associated protein-2, as well as neurofilament protein 200, synaptophysin, neuron specific enolase, substance P and chromogranin A + B. All these substances were found in Leydig cells of all sections independently of the pathological changes of the testes. Compared with the control cases, all the other groups showed a significantly weaker immunoreactivity for all markers. The uniformity of staining among the different antibodies allows the deduction that these neuroactive peptides may belong to a basic equipment of Leydig cells probably stabilizing their function in an autocrine manner. On the other hand, Leydig cells themselves seem to be a stable structural component of the testis, which are not essentially involved in the pathogenesis of the disturbances mentioned above.
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PMID:Neuroendocrine marker substances in human Leydig cells--changes by disturbances of testicular function. 790 79


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