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)

An important component of neuronal development is the matching of neurotransmitter expression with the appropriate target cell. We have examined how peptide transmitter expression is controlled in a simple model system, the avian ciliary ganglion (CG). This parasympathetic ganglion contains 2 distinct types of neurons: choroid neurons, which project to vasculature in the eye's choroid layer and use somatostatin as a co-transmitter with ACh, and ciliary neurons, which innervate the ciliary body and iris and use ACh but no known peptide co-transmitter. We have found that the earliest developmental stage in which neurons with somatostatinlike immunoreactivity (SOM-IR) are consistently found in vivo is stage 30 (embryonic day 6.5), a time shortly after the extension of neurites to targets in the eye's choroid layer. In cell culture, CG neurons expressed SOM-IR in co-culture with choroid cells, but not when cultured with striated muscle myotubes or with ganglion non-neuronal cells. No significant differences in neuronal survival or in ChAT activity were observed under these different co-culture conditions, which suggests that somatostatin expression is independently regulated. The stimulation of somatostatin expression was also specific in that other neuropeptides commonly found in autonomic neurons [neuropeptide Y (NPY), substance P (SP), vasoactive intestinal polypeptide (VIP)] were not induced in the presence of choroid cells. The ability to stimulate SOM-IR was not contact dependent because a macromolecule of greater than or equal to 10 kDa in choroid-conditioned medium (ChCM) was found to stimulate somatostatin expression in a dosage-dependent fashion. The somatostatin-stimulating activity induced SOM-IR in more than 90% of CG neurons, as well as in retrogradely labeled ciliary neurons, which would not normally express SOM-IR. Thus, the expression of somatostatin in cultured CG neurons is regulated by a macromolecule produced by cells in the choroid layer, a target normally innervated in vivo by CG neurons expressing somatostatin.
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PMID:Stimulation of somatostatin expression in developing ciliary ganglion neurons by cells of the choroid layer. 167 9

Substance P (SP) in the dose range 0.75-1.5 nmol exerts a potent stimulatory effect on ventilation after microinjection into the rat ventrolateral medulla oblongata (VLM; n. reticularis lateralis, n. paragigantocellularis lateralis). A significant but less pronounced effect is also seen in the dorsal medulla (DM; n. tractus solitarius). Somatostatin (0.6-1.8 nmol) inhibited ventilation and induced apnoea after microinjection into the VLM but not the DM. Serial microinjections of the two peptides showed a reciprocal antagonistic action in the VLM but not in the DM. The apnoea-inducing effect of SOM was blunted by SP while SOM reduced the ventilatory stimulation induced by SP. Extracellular single unit recordings were performed following the microiontophoretic application of SP and/or SOM to respiratory-related and non-respiratory-related neurons in the VLM and DM. Although a heterogeneous population of neurons were recorded from, the majority of respiratory-related units in the VLM responded with excitation to SP and inhibitory to SOM. A direct interaction between the peptides was seen in some respiratory-related units. The neurons not responding to either of the peptides were usually non-respiratory. Dorsal to the VLM, the type of response to the two peptides was less likely to be antagonistic and a wider distribution of response types were recorded. The results indicate a direct physiological antagonism between SP and SOM regarding their effects on respiratory regulation elicited in the VLM.
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PMID:Antagonistic effects of somatostatin and substance P on respiratory regulation in the rat ventrolateral medulla oblongata. 171 56

In situ hybridization was used to study the expression of prepro-neuropeptide Y (NPY), preprosomatostatin (SOM), preprotachykinin (PPT) and preprocholecystokinin (CCK) mRNA in caudate-putamen and frontoparietal cortex of rat brain with unilateral lesion of midbrain dopamine neurons. Neurons expressing NPY and SOM mRNA showed a similar distribution and the expression of both NPY and SOM appears to be regulated by dopamine in a similar fashion. Following a dopamine deafferentation, the numerical density of both NPY and SOM mRNA producing neurons almost doubled in the lesioned caudate-putamen with no change in the average grain density over positive neurons. Hence, in the intact caudate-putamen dopamine appears to suppress expression of these two neuropeptide genes leading to an activation of both NPY and SOM mRNA expression in many non- or low-expressing neurons when the level of dopamine is decreased. In the fronto-parietal cortex, on the other hand, dopamine appears to stimulate NPY and SOM gene expression. Thus, in the absence of dopamine about half of the NPY positive neurons disappeared. However, for SOM the number of positive neurons did not change, but rather most positive neurons appeared to have down-regulated their SOM mRNA expression. No evidence was found for a change in CCK mRNA expression by the dopamine deafferentation, while PPT mRNA expression decreased in the deafferented caudate-putamen. Consequently, dopamine exerts dissimilar effects on the expression of different neuropeptide genes, that in turn do not respond in the same way in different brain regions.
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PMID:Neuropeptide gene expression in brain is differentially regulated by midbrain dopamine neurons. 238 50

The effect of streptozotocin treatment (65 mg/kg i.v.) on plasma protein extravasation, nociception, and the content of substance P immunoreactivity (SP-IR) and somatostatin immunoreactivity (SOM-IR) was investigated in the rat. Twelve days after treatment, the neurogenic plasma extravasation induced by 5% mustard oil was reduced by 67% in the skin of the hind paw. Extravasation caused by SP, a putative mediator of neurogenic inflammation, was also reduced by 61% in the abdominal skin. While calcitonin gene-related peptide (CGRP) potentiated the SP-induced extravasation in control rats, no potentiation was observed in diabetic rats. Thermonociception or chemonociception was unchanged after streptozotocin treatment. The content of SP-IR and SOM-IR in sensory nerves or spinal ganglia was also not altered. These results indicate that the impairment of neurogenic inflammation in diabetic rats is not the result of depletion of neurogenic mediators like SP. Changes of the microvasculature at the leakage site appear to account for the effects observed.
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PMID:Reduced neurogenic inflammation in streptozotocin-diabetic rats due to microvascular changes but not to substance P depletion. 241 65

The peptidergic innervation of the human and guinea pig uterus was studied using immunohistochemical methods. Antibodies against several peptides were applied for the PAP-technique to stain peptidergic nerves specifically. These are located in the adventitia of large uterine vessels in the myometrium and smaller vessels of the myometrium and endometrium. A differential distribution of the individual peptides was observed for VIP-IR (vasoactive intestinal polypeptide immunoreactivity), NPY-IR (neuropeptide Y), SP-IR (substance P), SOM-IR (somatostatin) and NT-IR (neurotensin) nerve fibers. Specific functional implications for these neuropeptides can be derived from their histochemical location.
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PMID:Peptidergic innervation of the human and guinea pig uterus. 242 49

Immunohistochemical methods have been used to study the occurrence of neuronal markers in human gingiva from periodontitis-affected sites. In periodontitis-affected buccal gingiva densely distributed neurofilament (NF)-immunoreactive (IR) fiber bundles were observed in the deeper parts of the propria, while NF-IR single fibers occurred in the superficial propria and occasionally in the buccal epithelium. Periodontitis-affected gingiva obtained from interproximal sites showed only sparsely distributed NF-IR fibers. Single nerve fibers immuno-reactive to the peptides substance P and calcitonin gene-related peptide occurred close to or within the epithelium in both buccal and interproximal gingiva. Around blood vessels neuropeptide Y-, peptide histidine-isoleucine amide- and vasoactive intestinal polypeptide-IR fibers were occasionally observed, while clusters of gamma-melanocyte-stimulating hormone-IR cells were found in the propria, in addition to gamma-melanocyte-stimulating hormone IR nerve fibers. Somatostatin-IR dendritic cells were seen in epithelium and propria of buccal and interproximal gingiva, although a high variability in the number of SOM-IR cells was observed. All neuronal markers studied showed a similar distribution in material obtained from young patients with clinically healthy gingivae, although the number of NF-IR fibers in the propria in these subjects was lower. The results demonstrate that in gingiva obtained from periodontitis-affected sites several different biologically active peptides occur in both nerve fibers and cells. At least some of these substances could possible play a role in the inflammatory process. However, since clinically normal gingiva was shown to contain nerve fibers and cells expressing immunoreactivity to the substances studied, no unique periodontitis-induced expression of the neuronal markers studied was found. Thus, any alteration of these substances during the periodontitis process remains to be elucidated.
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PMID:Immunohistochemical study of neurochemical markers in gingiva obtained from periodontitis-affected sites. 257 Aug 28

The human brain contains several peptides with probable synaptic actions, some of which form complex neuronal networks in the limbic lobe (amygdala, hippocampus and temporal cortex). A limbic lobe abnormality has been postulated in schizophrenia on the basis of similarities between schizophrenic symptoms and symptoms in cases of known limbic pathology. Cholecystokinin (CCK), somatostatin (SRIF), neurotensin (NT), vasoactive intestinal polypeptide (VIP) and substance P (SP)-like immunoreactivities were measured by radioimmunoassay in 10 brain areas of 14 schizophrenics and 12 controls. In the schizophrenic group symptoms had been rated in life and the group was divided into Type I (n = 7) and Type II (n = 7) subgroups on the basis of the absence or presence of morbid negative symptoms. In control brains each peptide showed a characteristic distribution with high levels in cortex (CCK), limbic lobe (SOM, NT, VIP) or striatal areas (SP) and low levels of each of the peptides in thalamus. Significant (P less than 0.05) differences between groups were: reductions of CCK and SOM in hippocampus and CCK in amygdala in Type II schizophrenics, and CCK in the temporal cortex of the total schizophrenic group; and elevations of VIP in amygdala in Type I schizophrenics and of SP in the hippocampus in the total schizophrenic group. The findings could not be explained by variables such as age, delay between death and necropsy or to neuroleptic medication. These clinical-state related alterations in the peptide content of the limbic system in schizophrenia may illuminate the pathophysiological basis of the disease, particularly the distinction between Type I and II syndromes.
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PMID:Peptides, the limbic lobe and schizophrenia. 619 24

Two distinct carboxy-terminus-directed anti-substance P (SP) sera (R-1C and R-6G) were used to characterize immunoreactive SP (I-SP) in acetic acid extracts of anterior pituitary (AP) and posterior pituitary (PP) glands of adult male rats. The tissue concentrations of I-SP measured by R-1C and R-6G were comparable. The contents of I-SP were 600-1150 pg/AP and 25-52 pg/PP. I-luteinizing hormone releasing hormone and I-somatostatin (I-SOM) were undetectable in AP extracts, but PP extracts contained the equivalents of 325-785 pg I-SOM/gland. Serial dilutions of AP and PP extracts produced displacement curves with both SP antisera that were parallel to the respective synthetic SP standard and hypothalamic extract displacement curves. Gel filtrations of AP and PP extracts on a Sephadex G-25 column produced I-SP peaks eluting in the same fractions as synthetic SP and hypothalamic I-SP. However, the AP I-SP profile also revealed a side peak migrating between the void volume and the major I-SP peak. Neither immunoreactive species in the AP extract were eliminated when eluted with 6.0 M guanidine HCl, a strong denaturing agent. In vitro incubation of paired anterior hemipituitaries for 30 min in the presence of a 56 mM K+ concentration resulted in a significant (p less than .0001), 25-fold increase in the release of I-SP into the incubation medium above the mean control value. Radiofrequency lesions placed in the median eminence-arcuate region of male rats caused a significant (p less than .001) reduction of I-SP in both the AP and PP. These reductions were inversely related to the plasma prolactin values. The elevation in plasma prolactin was taken as an index of completeness of lesions. We conclude that: 1) the rat pituitary contains I-SP as assessed by its immunologic and chromatographic behavior, 2) K+ depolarization is a potent stimulator of the release of AP I-SP in vitro, 3) the ME-arcuate region is important for the maintenance of pituitary I-SP levels in the rat.
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PMID:Partial characterization of immunoreactive substance P in the rat pituitary gland. 619 79

The localization of substance P-(SP-), methionine-enkephalin (met-Enk-) and somatostatin (SOM-)like immunoreactivity was studied in the cat pyloric sphincter, ileum, ileocecal sphincter and proximal colon. The enteric plexuses in all regions examined contained SP-, met-Enk- and SOM-like immunoreactive varicose nerve fibres. A large number of especially SP- and met-Enk-containing varicosities were often seen to encircle the nerve cell bodies and processes in the two ganglionic plexuses. The SOM-like immunoreactive perikarya were the only peptide-containing nerve cells, preferentially located in the submucous ganglia. The predominant localization of the SOM-like immunoreactive neurons in the two enteric plexuses of the ileum was the most pronounced regional difference in the distribution pattern of the peptides. Among the layers of the cat intestinal wall the circular muscle contained the most peptide-immunoreactive fibres in contrast to the longitudinal muscle. Evidence was obtained for the occurrence of single peptide-immunoreactive varicose nerve fibres in muscularis mucosae as well as around the glands and the blood vessels. Immunoreactive endocrine cells occurred mainly in the ileum mucosa.
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PMID:Immunocytochemical localization of substance P, methionine-enkephalin and somatostatin in the cat intestinal wall. 620 22

Using the indirect immunofluorescence method, the distribution of galanin (GAL)- and galanin message-associated peptide (GMAP)-like immunoreactivities (LI) were studied in sympathetic ganglia and the adrenal gland of the guinea pig. A rather dense network of GAL-immunoreactive nerve fibers was found in the inferior mesenteric ganglion (IMG) and in the superior mesenteric pole of the celiac-superior mesenteric ganglion complex (C-SMG). The celiac pole of the C-SMG, the stellate ganglion, and the superior cervical ganglion contained fewer, mostly scattered fibers. SIF-cells in prevertebral and paravertebral ganglia contained GAL-LI, as did the adrenal medullary cells. The GAL fibers in the IMG surrounded mainly principal ganglion cells containing somatostatin-immunoreactivity (SOM-IR), whereas fewer fibers were seen around neuropeptide Y (NPY) cells and cells in which SOM and NPY coexisted. Application of colchicine or vinblastine onto the IMG did not result in the appearance of GAL-IR in the principal ganglion cells. In denervation experiments it was revealed that most of the GAL fibers reach the IMG via the lumbar splanchnic nerves. GAL-IR appears to be colocalized with substance P (SP) in fibers of the IMG, indicating an origin of the GAL-containing fibers in dorsal root ganglia (DRG). This conclusion was supported by the finding in lumbar DRGs of GAL-positive cell bodies that contained SP. The role of GAL in prevertebral ganglia is unclear. It may be suggested that GAL modulates the slow, long-lasting membrane depolarization of the principal ganglion cells caused by SP in the primary afferents related to the IMG. GMAP-LI was detected in SIF cells and adrenal medullary cells in which GMAP-LI parallels the immunoreactivity of GAL. GMAP-LI was not observed in neuronal cell bodies or nerve fibers of the ganglia.
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PMID:Immunohistochemical demonstration of galanin-, and galanin message-associated peptide-like immunoreactivities in sympathetic ganglia and adrenal gland of the guinea pig. 752 69


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