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)

Microelectrophoretic administration of D-alpha-aminoadipate reversibly reduced excitatory responses of cat dorsal horn neurones evoked by iontophoretic glutamate and non-noxious peripheral stimuli but did not influence similar responses evoked by noxious peripheral stimuli or iontophoretic substance P.
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PMID:Effects of D-alpha-aminoadipate on physiologically evoked responses of cat dorsal horn neurones. 44 14

In cats, under Dial anaesthesia, Renshaw cells were excited by microiontophoretic applications of acetylcholine (ACh), aspartate, and glutamate. Substance P, in small doses (10-30 nA), selectively abolished the responses to ACh, leaving the discharges evoked by the amino acids unchanged or enhanced. Higher doses (greater than 50 nA) depressed all responses, but those evoked by amino acids went down last and recovered sooner. By contrast, neither synaptic responses to ventral root stimulation nor spontaneous discharges were affected by substance P, presumably owing to the high efficacy of synaptic transmission and the presence of diffusion barriers around junctional sites.
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PMID:Substance P selectively blocks excitation of Renshaw cell by acetylcholine. 90 69

A peptide that exerts a depolarizing action on frog spinal motoneurons was found in the dorsal root of bovine spinal nerve. Pharmacological, chemical, and immunological properties of this motoneuron-depolarizing peptide were investigated and the results indicated that the peptide is identical with an undecapeptide, substance P, recently isolated from bovine hypothalamus by M.M. Chang and S.E.Leeman. The amount of hypothalamic substance P in bovine dorsal root determined by bioassay or radioimmunoassay was 24-130 pmole/g wet wt, whereas that in the ventral root was 9-27 times less. The effects of synthetic hypothalamic substance P on the isolated spinal cord of the frog and the newborn rat were studied. The peptide exerted a powerful depolarizing action on the motoneurons, its potency being about 200 times higher than that of L-glutamate. Distribution of substance P in the cat spinal cord was studied. The concentration of the peptide was highest in the dorsal part of dy lowered. When the dorsal root of the cat was ligated, substance P accumulated in a high concentration on the ganglion side of the ligature. These results, taken together, support the hypothesis that hypothalamic substance P is an excitatory transmitter of primary afferent neurons.
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PMID:Hypothalamic substance P as a candidate for transmitter of primary afferent neurons. 115 55

Beta-(4-chlorophenyl)-GABA (Baclofen, Lioresal) antagonized the excitant actions of acetylcholine and substance P to comparable extents. L-glutamate-induced excitation was affected to a lesser extent. These findings do not support the suggestion that beta-(4-chlorophenyl)-GABA is a specific substance P antagonist.
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PMID:Is beta-(4-chlorophenyl)-GABA a specific antagonist of substance P on cerebral cortical neurons? 127 5

The neurokinin-1 receptor binds neurokinin peptides with the potency order of substance P > substance K > neurokinin B. Elucidating the molecular basis of differential peptide selectivity will require the localization of the binding domain on the receptor. In the present report, mutagenesis and heterologous expression experiments reveal that a segment of the extracellular N-terminal sequence of the neurokinin-1 receptor is required for the high-affinity binding of substance P and related peptide agonists. Substitution of amino acid residues in the N-terminal region of the receptor affects the binding affinity of both intact peptides and a C-terminal substance P "analog", but not of a nonpeptide antagonist. Glycosylation of the receptor does not change the peptide binding affinity. In addition, substitution of the valine-97 residue in the rat neurokinin-1 receptor by a glutamate residue increases the binding affinity of neurokinin B but not substance P or substance K, suggesting that the second extracellular segment is involved in peptide selectivity. These results indicate that the extracellular domains of neurokinin-1 receptor play a critical role in peptide binding.
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PMID:The extracellular domain of the neurokinin-1 receptor is required for high-affinity binding of peptides. 128 Jan 61

Huntington's disease is a progressive neurodegenerative disease in which the basal ganglia are preferentially affected. Recent evidence, however, suggests involvement of the cerebral cortex as well, with sparing of neurochemically defined subsets of gamma-aminobutyric acid (GABA)-ergic interneurons. In the present study, we examined changes in concentrations of the amino acid neurotransmitters GABA, glutamate, and aspartate in nine cortical regions from 23 patients with advanced Huntington's disease and 12 control brains. GABA concentrations were significantly increased in eight of the nine regions, consistent with a sparing of GABAergic local circuit neurons in the context of progressive cortical atrophy. Small but significant increases in glutamate were found in six of the nine regions, while aspartate levels were generally unaffected. Striate cortex (Brodmann's area 17) showed the most profound increases in GABA and glutamate. We also investigated the effects of powdering the excitotoxins N-methyl-D-aspartate (NMDA) or kainic acid onto the dura of rats. The resulting lesions were examined at 1 week and 6 months. The NMDA-induced lesions showed striking sparing of parvalbumin-positive neurons (a subset of GABAergic interneurons), and this sparing was reflected in neurochemical measurements of GABA; kainic acid lesions failed to display this selectivity. Somatostatin, cholecystokinin, and vasoactive intestinal polypeptide concentrations were spared by the NMDA-induced lesions, and substance P levels were significantly increased. These results provide evidence that NMDA excitotoxic lesions of cerebral cortex can produce a selective pattern of neuronal damage similar to that which occurs in Huntington's disease.
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PMID:The cortical lesion of Huntington's disease: further neurochemical characterization, and reproduction of some of the histological and neurochemical features by N-methyl-D-aspartate lesions of rat cortex. 128 Sep 37

The presence of glutamate (Glu), aspartate (Asp) and substance P (SP) in the petrosal ganglion of rats anesthetized with pentobarbital sodium was studied using retrograde labeling of the carotid sinus nerve (CSN) with horseradish peroxidase (HRP) in combination with immunohistochemistry. (i) The incidence of HRP/Glu-labeled cells was the highest (32%, n = 3), followed in order by HRP/Asp-labeled cells (23%, n = 3) and HRP/SP-labeled cells (6%, n = 3). (ii) No significant difference was observed in the average diameter of HRP/Glu- and HRP/Asp-labeled cells, but the average diameter of HRP/SP-labeled cells was significantly larger than that of HRP/Glu- and HRP/Asp-labeled cells (P < 0.01). These results suggest that Glu may coexist with Asp, and SP-containing cells may form a different population from Glu- and Asp-containing cells in the petrosal ganglion. The physiological role of these transmitter substances is discussed.
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PMID:Transmitter substances contained in the petrosal ganglion cells determined by a double-labeling method in the rat. 128 28

An immunocytochemical technique that allows visualization of two antigens in the same neuron was used to verify the possibility that some neocortical pyramidal neurons contain both glutamate (Glu) and substance P (SP) immunoreactivity. The results show that a large fraction of SP-positive pyramidal neurons are also Glu-positive, and indicate that in a small population of cortical neurons a fast excitatory synaptic transmitter and a slow peptidic modulator coexist.
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PMID:Numerous SP-positive pyramidal neurons in cat neocortex are glutamate-positive. 128 58

Intracellular recordings from sympathetic preganglionic neurons (SPNs) in adult cat and neonatal rat spinal cord slices reveal four types of synaptic potentials, namely, excitatory postsynaptic potentials (EPSPs), inhibitory postsynaptic potentials (IPSPs), and slow EPSPs in both preparations, and a slow IPSP in cat SPNs. Pharmacological studies show that glutamate or a related excitatory amino acid and glycine are the probable mediators of EPSPs and IPSPs. There may be heterogenous mediators of slow EPSPs; substance P, serotonin, norepinephrine, and epinephrine are all probable mediators of slow EPSPs in subpopulations of SPNs. In the case of slow IPSPs, norepinephrine appears to be the likely transmitter. Finally, stimulation of ventral roots elicits a synaptic potential that appears to be caused by glutamate released from afferent fibers in the ventral roots. Our results indicate that a multitude of synaptic mechanisms exist in the rat SPNs by means of which inputs arising from sensory and supraspinal neurons are processed in a timely and orderly manner, thus ensuring highly organized but differentiated outputs to multiple peripheral target cells.
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PMID:Synaptic mechanisms in sympathetic preganglionic neurons. 129 89

The receptor agonist-mediated hydrolysis of phosphoinositides and production of prostacyclin were studied in murine cerebral endothelial cells (MCEC). Of 11 neurotransmitters and neuromodulators examined, carbachol, noradrenaline (NE), bradykinin, and thrombin significantly increased 3H-inositol phosphate accumulation in the presence of LiCl (20 mM). The maximal stimulation of [3H]inositol monophosphate ([3H]IP1) reached approximately 11, 11, seven, and four times the basal levels for carbachol, NE, bradykinin, and thrombin, respectively. The EC50 values of IP1 accumulation for carbachol and NE were 34 and 0.16 microM, respectively. The muscarinic antagonists, atropine and pirenzepine, blocked the carbachol-induced IP1 accumulation with Ki values of 0.3 and 30 nM, respectively. The adrenergic antagonist, prazosin, blocked NE-induced IP1 accumulation with a Ki of 0.1 nM. The calcium ionophore A23187, histamine, glutamate, vasopressin, serotonin, platelet activating factor, and substance P did not stimulate IP1 accumulation. A23187, bradykinin, and thrombin stimulated prostacyclin release to approximately four, four, and two times the basal levels, respectively, whereas carbachol and NE had little effect upon prostacyclin release. These results suggest that the activation of phospholipase C and of phospholipase A2 in MCEC are regulated separately.
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PMID:Receptor-linked hydrolysis of phosphoinositides and production of prostacyclin in cerebral endothelial cells. 131 55


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