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)

Extracellular and intracellular recordings were made in vitro from single neurons of the myenteric plexus of the guinea-pig small intestine. Synthetic substance P was applied to the neurons by means of the perfusing solution or by electrophoresis from micropipettes. Extracellular recording showed that substance P (100 pm-30 nm), applied by perfusion, increased the firing rate of myenteric neurons. Intracellular recording indicated that perfusion with substance P caused a dose-dependent membrane depolarization which was unaffected by hexamethonium, hyoscine, naloxone or baclofen. The depolarization was also evoked by electrophoretic application of substance P. It was associated with an increase in membrane resistance, augmented by membrane depolarization and reduced by membrane hyperpolarization. The relation between the substance P reversal potential and the logarithm of the extracellular potassium concentration was linear with a slope of 54 mV/log10[K+], which indicates that substance P inactivates the resting potassium conductance of the myenteric neurons. This effect on ion conductance is the same as that of an unknown substance that mediates slow synaptic excitations with the myenteric plexus.
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PMID:The action of substance P on neurons of the myenteric plexus of the guinea-pig small intestine. 4 23

Push-pull cannuale were implanted into the substantia nigra (SN) and the caudate nucleus (CN) of the cat to study the in vivo release of substance P (SP), using a radioimmunoassay and high pressure liquid chromatography (HPLC) analysis. The spontaneous release of SP could be detected in the SN and the CN. Potassium (50 mM) locally applied stimulated SP release in both structures. Furthermore an important evoked release of SP was observed in the SN during depolarization of striato-nigral SP fibers with potassium (50 mM) applied in the CN.
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PMID:In vivo release of substance P in the cat substantia nigra. 9 29

The possibility that L-glutamate is the excitatory transmitter at the Drosophila larval neuromuscular junction and the ionic basis of its action on the muscle membrane are examined. 2. Iontophoretically applied L-glutamate causes muscle depolarization (L-glutamate potential) if and only if the L-glutamate pipette is within a few mum of the nerve ending. D-glutamate, substance P, ACh and GABA are ineffective. 3. Bath-applied L-glutamate produces similar changes in the time course and amplitude of miniature excitatory junctional potential (m.e.j.p.), excitatory junctional potential (e.j.p.) and the L-glutamate potential. 4. Neuromuscular transmission and excitation-contraction coupling are operative in a haemolymph-like solution containing 1 mM L-glutamate. 5. The reversal potentials of the e.j.p. and the L-glutamate potential are identical to each other, changing similarly with changes in the ionic compositions of the external medium (twelve solutions). 6. The ionic dependence of the reversal potentials is predicted from an extended constant-field equation using a ratio of sodium:potassium permeabilities of PNa/PK=1-3, and a ratio of magnesium:potassium permeabilities of PMg/PK=4-7. 7. It is concluded that L-glutamate is, or is an agonist of, the excitatory transmitter at certain Drosophila larval neuromuscular junctions.
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PMID:L-glutamate as an excitatory transmitter at the Drosophila larval neuromuscular junction. 18 87

Effect of methionine-, leucine-enkephalin (met-, leu-enkephalin) and substance P on the transmission in mouse vas deferens was studied. Both met- and leu-enkephalin inhibited electrically induced contraction of vas deferens at 10(-8)-10(7) M, met-enkephalin being 1.4 times more active than leu-enkephalin. Nalorphine (10(-6) M) antagonized these effects. Substance P (10(-9)-10(-7) M) had no effect on the contraction. Met- and leu-enkephalin (10(-7)-10(-5) M) decreased the high potassium induced [3H]-norepinephrine release from vas deferens, while substance P (10(-6) M) significantly increased it. Nalorphine (10(-5) M) reversed the inhibitory effect of met-enkephalin. These results indicate that these peptides modify the transmission of sympathetic nerve in mouse vas deferens.
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PMID:Effect of enkephalin and substance P on sympathetic nerve transmission in mouse vas deferens. 20 50

1. Substance P (synthetic or extracted for intestine or central nervous system) is devoid of an algesic effect on paravascular pain receptors. 2. The algesic effect of a AP-containing acetone HCl-extract from spinal cord is explained by its high content of potassium ions. 3. SP-containing preparations which include an ammonium sulphate precipitation in the extraction procedure are algesic due to content of this salt. 4. SP-containing extract from intestine were found to be contaminated with a bradykinin-like peptide of high algesic potency. 5. These findings are discussed with regard to the restricted value of earlier results about central actions of SP-containing tissue extracts and with regard to the role of SP as a possible neurotransmitter.
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PMID:Lack of algesic effect of substance P on paravascular pain receptors. 56 91

1. Rat brain synaptosomes were incubated under different conditions to study the release of substance P (SP). 2. Potassium ions and electrical field stimulation induced a loss of SP from synaptosomes. The release of SP by potassium in high concentrations (23.8 mM) was shown to be calcium dependent. 3. Substance P was retained in synaptosomes during incubation in 0.32 M sucrose at +4 degrees C up to 120 min. During incubation at 30 degrees C the SP content fell initially (30 min) but was gradually restored (120 min). 4. If these pre-incubated synaptosomes were reincubated for 45 min at 30 degrees C in potassium free Krebs-Ringer-phosphate buffer a further rise in their SP content occurred which was taken as indication that SP is being synthesized in synaptosomes. 5. The newly synthesized SP is presumably stored by binding to phosphatidyl serine until a sudden release is initiated by depolarization.
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PMID:Substance P in rat brain synaptosomes. 60 Mar 16

The characteristics of substance P release have been investigated in the rat substantia nigra, in vitro, using a sensitive radioimmunoassay method. The spontaneous efflux of substance P represented approximately 0.5% of tissue stores released per minute. Addition of potassium to the superfusion medium produced a concentration-dependent increase in substance P release which was linear over the range 15--60 mM potassium. The potassium-evoked release of substance P was almost totally abolished by removal of calcium from the superfusion medium, and was linearly related to an increase in calcium concentration with a corresponding decrease in the magnesium concentrations over the range 0.1--3.0 mM calcium. Veratridine (50 micrometer) also evoked the release of substance P in a calcium- and tetrodotoxin-sensitive manner. Superfusion of substantia nigra slices with GABA produced a concentration-dependent inhibition in the K+-evoked release of substance P which could be abolished by continuous superfusion with picrotoxin. Bicuculline was less effective than picrotoxin in blocking the effects of GABA. The GABA agonist muscimol also produced an inhibition of substance P release, whereas baclofen was without effect. These results support the concept that substance P may function as a neurotransmitter within the substantia nigra, and suggest that GABA may have a role in the regulation of substance P release.
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PMID:Substance P release from the rat substantia nigra. 66 25

The effects of GABA, substance P and dopamine on the release of newly synthesized 3H-5-HT were investigated, using slices of rat substantia nigra superfused with L-3H-tryptophan in vitro. GABA (50 micron) had no inhibitory effect on the potassium-evoked-release of 3H-5-HT. Substance P (50 micron) and eledoisin (50 micron) stimulated the spontaneous release of 3H-5-HT. This effect seems to be indirect and is possibly mediated by dopaminergic neurones, since the dopamine antagonist drug alpha-flupenthixol (1 micron) abolished the substance P-evoked release of 5-HT. Furthermore, it was found that substance P (10 micron) stimulated 3H-dopamine release from nigral slices in vitro and the dopaminergic agonist apomorphine (50 micron) also stimulated 3H-5-HT release. Substance P may, therefore, activate nigral dopaminergic neurones which then release dopamine from their dendrites. The release of dopamine may in turn stimulate 5-HT release from terminals of the raphe-nigral pathway.
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PMID:Effects of GABA, dopamine, and substance P on the release of newly synthesized 3H-5-hydroxytryptamine from rat substantia nigra in vitro. 71 84

Crude mitochondrial P2 fractions from bovine hypothalamus and substantia nigra, slices from rabbit spinal cord and mesencephalon and glial fractions from rabbit brain were incubated with [3H]-substance P and the uptake was measured and compared with those for 5-HT and GABA. Substance P was to some extent taken up into the fractions but this uptake was neither temperature nor time dependent and the pellet/medium ratios were less than 1. Similar results were obtained in high potassium treated slices from rabbit mesencephalon. The rate of uptake for [3H]-substance P increased linearly in proportion to the medium concentration, suggesting a non-saturable binding. These results, together with our previous observations provide strong evidence that nerve terminals and glial cells lack a temperature sensitive, active uptake system capable of terminating transmitter action of substance P at the synapse.
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PMID:Further observation on the lack of active uptake system for substance P in the central nervous system. 92 60

Whole-cell recordings were made from neurons of the rat locus coeruleus in a tissue slice removed from rat brain. Substance P caused an inward current in cells voltage-clamped at -60 mV. The effect of substance P was concentration-dependent (30 nM-3 microM) and was mimicked by similar concentrations of substance K and neuromedin K. The inward current resulted predominantly from an increase in membrane cation conductance; in potassium-free solutions it reversed polarity at about 12 mV. Substance P also reduced the conductance of an inwardly rectifying potassium current; this action was studied with low external sodium concentration. It is concluded that substance P excites rat locus coeruleus neurons by activating an intracellular transduction pathway leading to both cation conductance increase and potassium conductance decrease.
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PMID:Substance P opens cation channels and closes potassium channels in rat locus coeruleus neurons. 127 60


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