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)

beta-endorphin-like immunoreactivity (BE-li), methionine enkephalin-like immunoreactivity (ME-li), and substance P-like immunoreactivity (SP-li) were measured in the posterior pituitary of rats that experienced a 5-day space flight in a Space Shuttle. ME-li and SP-li were both significantly lower compared to the control rats. However, there was no difference in BE-li between flight and control rats. These data suggest that the space flight stress diminished the methionine enkephalin (ME) and substance P (SP) concentrations in the posterior pituitary without affecting the beta-endorphin (BE) concentration. Thus, the proenkephalin A and tachykinin, but not proopiomelanocortin, neuropeptidergic systems in the posterior pituitary may respond to this type of unique stress.
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PMID:Effects of space flight stress on proopiomelanocortin, proenkephalin A, and tachykinin neuropeptidergic systems in the rat posterior pituitary. 751 53

A large number of neurotransmitters and neuropeptides are concentrated in the dorsal horn of the spinal cord, where they interact in a complex manner and modulate sensory mechanisms. Most studies are carried out in the rat, and little is known of other species. It is relevant to study mammals with a more complex central nervous system, because pain mechanisms are central in both human and veterinary medicine. Immunoreactivity for neuropeptide FF, an amidated octapeptide originally isolated from bovine brain, was found immunocytochemically at all levels of porcine spinal cord. In contrast to other species studied so far, the peptide immunoreactivity in porcine spinal cord was confined to the intermediolateral gray matter, especially to the intermediolateral cell column and lamina X of the gray matter. This distribution was remarkably different from that of substance P, proenkephalin A-derived peptides, thyrotropin-releasing hormone, serotonin, and neuropeptide Y. Pharmacologic administration of neuropeptide FF alters behavior in assays for analgesia. The distribution of neuropeptide FF immunoreactivity as revealed by this study suggests that there may be marked species differences in the distribution and function of the peptide.
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PMID:Distribution of neuropeptide FF in porcine spinal cord in comparison with other neuropeptides and serotonin. 752 61

Activation of c-fos, a member of the class of immediate early genes that act as transcription factors, may be one of the initial molecular mechanisms underlying plastic changes in gene expression in response to drugs of abuse. By combining c-fos (radioactive) in situ hybridization histochemistry with nonradioactive in situ hybridization histochemistry for mRNAs encoding other striatal markers [preprotachykinin (substance P), proenkephalin, and D1 and D2 receptors], we have identified the cellular phenotype of striatal neurons activated by acute administration of cocaine to P8, P15, P28, and adult rats. At each age examined, substance P+, enkephalin- striatal neurons were the predominant class of cells in which cocaine induced c-fos gene expression. In addition, the topography of cellular activation at each age examined was distinct and reflected the topography of distribution of cells expressing high levels of substance P mRNA. We conclude that there is a marked specificity of cellular activation in striatum following acute cocaine administration restricted predominantly to subsets of substance P-expressing cells, with age-specific patterns in their topographic distribution.
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PMID:Substance P phenotype defines specificity of c-fos induction by cocaine in developing rat striatum. 753 74

To study the comparative development of the two major neuropeptide genes of the striatum, we used immunocytochemistry to detect immunoreactivity (ir) for substance P and synenkephalin (the N terminus of proenkephalin), and in situ hybridization to detect proenkephalin mRNA. Earliest detection of substance P-ir was in the anlage of the bed nucleus of the stria terminalis (BST, at E15) and in the rostral-lateral caudate-putamen (CPu), at E16. Substance P in the BST was immediately subjacent to the medial ganglionic eminence, while immunoreactivity in the CPu was associated with the lateral ganglionic eminence. Earliest detection of synenkephalin-ir or proenkephalin mRNA was in the caudal-lateral CPu and the adjacent central nucleus of the amygdala (Ce), at E16. Over the next several days, expression of each neuropeptide spread toward the region of first expression of the other neuropeptide. The first overlap of expression of the two neuropeptides was at E18, at the level of the septum. Despite correspondence of substance P-ir and proenkephalin mRNA in patches at P0, very little co-expression of the two neuropeptides was evident in individual neurons. We propose a model in which the CPu develops primarily from the lateral ganglionic eminence, and the extended amygdala develops primarily from the medial ganglionic eminence. Within each structure, two poles of neuropeptide gene expression are established initially: substance P-ir in the rostral CPu and in the rostral-medial pole of the extended amygdala (represented by the BST), and synenkephalin/proenkephalin in the caudal CPu and in the caudal-lateral pole of the extended amygdala (represented by the Ce). A stream of substance P-ir cells connects the two poles of the extended amygdala, in the sublenticular substantia innominata.
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PMID:The development of enkephalin and substance P neurons in the basal ganglia: insights into neostriatal compartments and the extended amygdala. 753 4

Disruption of dopaminergic neurotransmission in the striatum by neurotoxic lesions of the substantia nigra leads to increases in glutamic acid decarboxylase and proenkephalin messenger RNA expression, and to decreases in preprotackykinin (the precursor molecule for substance P) messenger RNA expression in the two populations of striatal medium-sized spiny projection neurons. These cells also express TrkB, the neurotrophin receptor for brain-derived neurotrophic factor and neurotrophin 4/5, and TrkC, the receptor for neurotrophin-3. Since there is some indication that exogenous brain-derived neurotrophic factor can exert neuromodulatory effects in the basal ganglia, we studied the effects of repeated intrastriatal injections of the four members of the neurotrophin family of neural growth factors, nerve growth factor, brain-derived neurotrophic factor, neurotrophin-3, and neurotrophin-4/5 on the expression of striatal neurotransmitter-related genes in the unilaterally 6-hydroxydopamine-lesioned rat using in situ hybridization histochemistry. We found that 4 micrograms/day of brain-derived neurotrophic factor or neurotrophin-4/5 when injected intrastriatally for eight consecutive days led to a normalization of the denervation-induced decrease of preprotachykinin messenger RNA when compared to animals injected with equivalent doses of nerve growth factor, neurotrophin-3, or vehicle. Neurotrophin-4/5 alone also normalized expression of messenger RNA encoding the 67 x 10(3) mol. wt isoform of glutamate decarboxylase, while none of the neurotrophins had a significant effect on preproenkephalin messenger RNA expression.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Brain-derived neurotrophic factor and neurotrophin-4/5 modify neurotransmitter-related gene expression in the 6-hydroxydopamine-lesioned rat striatum. 761 69

1. The aim of this study was to investigate the neurochemical effects and measure the anatomical spread of infusion of c-fos antisense (AS) DNA into the striatum. 2. Rats were anesthetized and infused in opposing striata with c-fos AS and c-fos sense (S) DNA. Ten hours later they were injected with apomorphine (2 mg/kg, i.p.) and 20 min later they were overdosed with sodium pentobarbital and their brains either perfused or frozen. Vibratome-cut sections were immunostained for the detection of c-fos, JunB, Krox 24, somatostatin, substance P, dynorphin, tyrosine hydroxylase, and enkephalin. Cryostat-cut sections from the caudate were immunostained for the detection of c-fos, JunB, and Krox 24, as well as in situ hybridization for proenkephalin mRNA. Sections from the globus pallidus were used for the autoradiographic localization of D2 dopamine and A2a adenosine receptors. Sections from the substantia nigra were used for the autoradiographic localization of D1 dopamine and cannabinoid receptors. A second group of rats were injected in opposing striata with biotin-labeled c-fos AS DNA and c-fos S DNA. Ten hours later they were challenged with apomorphine (2 mg/kg, i.p.) and 20 min later brains were either perfused or frozen. Sections from these brains were cut throughout the rostral-caudal extent of the forebrain and the biotin labeled AS DNA was localized. 3. Krox 24 was expressed at high levels on the sense side of the brain in the striatum and overlying neocortex. However, on the AS-injected side there was a reduction in Krox 24 expression in striatum and overlying cortex. The biotin-labeled AS studies confirmed that the striatal infusion spread throughout the dorsal striatum as well as the overlying neocortex. We did not detect any changes in neurotransmitter receptors, neuropeptides, or tyrosine hydroxylase in AS/S-injected rat brains. 4. These results demonstrate that c-fos AS reduces Krox 24 expression in striatal and neocortical neurons but does not change the expression of a number of other proteins involved in basal ganglia function. Whether this effect is due to nonspecific actions of c-fos AS or to its effects on a component of the transduction pathway responsible for basal Krox 24 expression (NMDA receptors?) is unknown.
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PMID:c-fos antisense reduces expression of Krox 24 in rat caudate and neocortex. 762 2

The opioidergic innervation of the mammalian spleen and possible species differences were investigated. Light-microscopic immunohistochemistry revealed that splenic nerves of bovine and porcine spleen, but not of rat, mouse, hamster and guinea-pig spleen contained proenkephalin-derived opioidergic innervation. Immunoreactivity to both prodynorphin and pro-opiomelanocortin was absent from splenic nerves. In bovine and porcine spleen, fibers immunoreactive for met-enkephalin, met-enkephalin-Arg-Phe, met-enkephalin-Arg-Gly-Leu, leu-enkephalin and peptide F formed perivascular plexus, traveled in trabecular connective tissue, and extended into the capsule. Spatial relationships with immune cells were apparent in the white and red pulp, excluding lymphoid follicles. Colocalization of enkephalin immunoreactivity with immunoreactivities for tyrosin hydroxylase, dopamin-beta-hydroxylase, and neuropeptide Y, but not for substance P or calcitonin gene-related peptide were found. Our results provide evidence that opioid expression in splenic innervation is strongly species-dependent and exclusively proenkephalin-derived. Colocalization with marker enzymes of noradrenergic neurons indicates a mainly postganglionic sympathetic origin of proenkephalinergic splenic innervation. Opioidergic perivascular nerves probably control the splenic blood flow. A close interrelationship of opioidergic fibers with immune cells provides the anatomical basis for direct effects of neurally released opioids on splenic immune functions.
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PMID:Pro-enkephalin opioid peptides are abundant in porcine and bovine splenic nerves, but absent from nerves of rat, mouse, hamster, and guinea-pig spleen. 762 19

Applying double-labelling immunofluorescence, the peptide content of solitary and clustered small intensely fluorescent (SIF) cells, identified by an antiserum to a selective membrane glycoprotein marker, synaptophysin, was correlated with the presence of catecholamines in the rat superior cervical ganglion. Most of synaptophysin-immunoreactive solitary and clustered SIF cells apparently contained dopamine (indicated by tyrosine hydroxylase-TH) but not noradrenaline (indicated by dopamine-beta-hydroxylase-DBH). Frequently, immunoreactivities for substance P or rarely, neuropeptide Y were colocalized in TH-immunolabeled cells of both types. Immunostaining for vasoactive intestinal polypeptide was found only in solitary SIF cells and was visible in TH-immunoreactive, as well as in TH-nonreactive cells. Very few solitary SIF cells were TH- and DBH-immunoreactive. Solitary and clustered SIF cells, as a rule, were encircled by leu-enkephalin-positive fibres which were also met-enkephalin-arg6-phe7-immunoreactive, indicating proenkephalin as precursor. SIF cells were additionally approached by varicose fibres which contained immunoreactivity for calcitonin gene-related peptide (CGRP) but not for enkephalins. As observed by immuno-electronmicroscopy, fibres that were immunostained for leu-enkephalin or CGRP, deeply invaginated into SIF cell somata. In addition to close membrane appositions, CGRP-immunolabeled fibres exhibited efferent synaptic contacts wih elements of SIF cell clusters. SIF cells were non-reactive to enkephalin-antisera in control ganglia and after transection of the postganglionic nerves (axotomy); but both types exhibited leu-enkephalin in preganglionically transected ganglia (decentralization) in which enkephalin-immunoreactive fibre baskets were absent. Synthesis of enkephalin in SIF cells after decentralization was confirmed by in situ hybridization demonstrating intracytoplasmic proenkephalin messenger-RNA. The findings are indicative for a differential neurochemical equipment of SIF cells in the rat superior cervical ganglion, which mainly is independent to a topographical classification. Moreover, they demonstrate the involvement of two neuropeptides in preganglionic SIF cell innervation. Finally, the observations indicate the capacity of SIF cells for proenkephalin-expression in response to preganglionic denervation.
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PMID:Neurochemistry, connectivity and plasticity of small intensely fluorescent (SIF) cells in the rat superior cervical ganglion. 768 94

Significant post-mortem changes in peptide concentration occur within the previously unstudied timeframe, i.e. within 1 h, for the proenkephalin A, proopiomelanoccortin, and tachykinin neuropeptidergic systems in the pituitary. These data differ from data obtained in other studies that concluded that peptides are stable for up to 72 h post-mortem. The post-mortem stability of the three neuropeptides, methionine enkephalin, substance P, and beta-endorphin, was studied in the rat pituitary to test the hypothesis that significant post-mortem concentration changes of those three neuropeptides occur in the immediate post-mortem time period.
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PMID:Methionine enkephalin-like immunoreactivity, substance P-like immunoreactivity and beta-endorphin-like immunoreactivity post-mortem stability in rat pituitary. 769 Jul 65

In a study to test the hypothesis that defects in the metabolism of neuropeptides might be a contributing factor to human anterior pituitary tumor formation, the proenkephalin A, proopiomelanocortin (POMC), and tachykinin systems, which produce methionine enkephalin (ME), beta-endorphin (BE), and substance P (SP), respectively, were measured in patients who had a wide variety of pituitary tumors. Mass spectrometry was used to optimize the level of molecular specificity of the ME and BE analytical measurements, and radioimmunoassay was used to measure SP-like immunoreactivity (SP-li). Compared to data obtained from pituitaries from post-mortem controls, the non-secreting tumors contained a significantly lower amount of the POMC neuropeptide, BE. The lower ME level was not significant. However, two adrenocorticotrophic hormone (ACTH)-secreting tumors contained ME, BE, and SP-li amounts that were much higher than both the controls and nonsecreting tumors. These data suggest that a hypometabolism of the POMC precursor may be operating in non-secreting tumors, and that a hypermetabolism of the proenkephalin A, POMC, and tachykinin precursors may be operating in two ACTH-secreting tumors. These data demonstrate that mass spectrometry plays a critical role in the study of human pituitary tumors.
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PMID:Mass spectrometric analysis of opioid and tachykinin neuropeptides in non-secreting and ACTH-secreting human pituitary adenomas. 838 75


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