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)

The anatomical and biochemical features of primary sensory afferents and the peptidergic innervation of cremaster motoneuron efferents in the genitofemoral (Gf) nerve were analyzed in the rat using immunohistochemical, histochemical, retrograde tracing and lesion methods. Afferent fibers in the Gf nerve were shown to originate from neurons in L1 and L2 dorsal root ganglia (DRG) and to project to L1 to T12.5 in the spinal cord. Some of the DRG neurons giving rise to these fibers contained substance P (SP) or the enzyme fluoride-resistant acid phosphatase but none appeared to contain somatostatin. The dermatome area of the Gf nerve, as determined by plasma extravasation methods, was located in the rostral scrotal and adjacent abdominal region. Identification of cremaster motoneurons by retrograde labelling from the Gf nerve revealed these neurons to be located in the L1 to L2 spinal cord segment, to have prominent rostrocaudally oriented dendritic aborizations and to receive a rich innervation by fibers containing SP, thyrotropin-releasing hormone (TRH) or met-enkephalin (met-Enk). Lesion studies indicated the SP-and met-Enk-containing fibers to be supplied by local intraspinal systems and the TRH-containing fibers by supraspinal systems. In female rats, motoneurons corresponding to the male version of the cremaster motoneuronal pool were less developed and received far fewer peptidergic connections than that observed in males. The multiple neural systems innervating cremaster motoneurons together with sensory afferents in the Gf and other scrotal nerves are suggested to be involved in the contribution of cremaster muscles to thermoregulation of the scrotum.
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PMID:Neural relations of cremaster motoneurons, spinal cord systems and the genitofemoral nerve in the rat. 393 95

1. An enzyme which can be extracted from brain inactivates nerveside in the optimum pH range 5.8-7.0.2. The polybasic acids trypan blue and its analogue trypan red, bromphenol blue and its analogue bromthymol blue at concentrations of 0.22 mM and ethylenediaminetetra-acetic acid (EDTA) at a concentration of 1 mM are strong inhibitors of the enzyme.3. Penicillin which is a monobasic carboxylic acid also inhibits the enzyme but only if concentrations as high as 3.6 mM are used. The antibiotic streptomycin which is a basic substance does not inhibit the enzyme.4. Caffeine at a concentration of 7.2 mM only weakly inhibits the enzyme.5. Chymotrypsin and wheat germ acid phosphatase also inactivate nerveside at pH 5.9 and are inhibited by the acidic dyes and penicillin. EDTA inhibits wheat germ phosphatase but activates chymotrypsin.6. Inactivation of nerveside by the brain enzyme and by wheat germ phosphatase is different from the action of chymotrypsin. Nerveside solutions incubated with chymotrypsin completely lose all biological activity whereas if incubation is carried out with either the brain enzyme or wheat germ acid phosphatase a residual biological activity remains even when the concentration of these two enzymes is increased. This residual biological activity is due to a peptide as it is destroyed by chymotrypsin.7. The manner in which nerveside is inactivated by the brain enzyme is uncertain as the preparation of the latter contained phosphodiesterase and protease activities which were similarly inhibited by the acid dyes, penicillin and EDTA.8. Pentylenetetrazole, picrotoxin, strychnine and tetanus toxin do not inhibit the brain enzyme.9. The nerveside-inactivating enzyme is not identical with the Substance P-inactivating enzyme in brain as the former is inhibited by EDTA while the latter is not.
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PMID:The inhibitory effect of convulsant agents on the enzyme in brain which inactivates nerveside. 439 Mar 85

Activation of cutaneous chemosensitive afferents results in the release of substances which increase the permeability of the microcirculation, producing inflammation. That this inflammation is neurogenic is readily demonstrated by antidromic electrical stimulation of afferent fibres. In the present study we have used the technique of dye extravasation to compare both qualitatively and quantitatively neurogenic extravasation skin and skeletal muscle. Plasma extravasation has been found to occur in skeletal muscle after stimulation but only at less than 10% of the levels seen in skin. We have also found that the levels of the C-fibre markers substance P and fluoride-resistant acid phosphatase are greatly reduced in muscle compared with skin nerves. These results show that there are substantial differences in the population of C-fibres supplying muscle compared with those supplying skin.
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PMID:Neurogenic extravasation and substance P levels are low in muscle as compared to skin the rat hindlimb. 608 9

The postnatal development of sensory C fibre function was investigated in neonatal rats aged 1-21 days. From birth, flexor-withdrawal reflexes (measured from the hamstring electromyograph) to pinching and heating the skin of the hindfoot were easily recorded under light anaesthesia and in fact were exaggerated in amplitude and duration compared to adult responses. Flexor reflexes to irritant chemicals, however, were not present until day 10-11 of life. In parallel with this late development of specific chemical sensitivity, neurogenic oedema, a C fibre-mediated inflammatory reaction, also did not occur until day 11. Substance P and fluoride-resistant acid phosphatase histochemistry were used to investigate the neurochemical development of sensory C fibres. Substance P was present in the skin, nerve, dorsal root ganglion and spinal cord from birth and fluoride-resistant acid phosphate within 12 h of birth. The adult neurochemical appearance of C-fibre terminals in the dorsal horn was established in a few days. The results show that despite the apparent early anatomical and neurochemical maturity of C fibres, physiological function is not fully established until the second week of life.
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PMID:The postnatal physiological and neurochemical development of peripheral sensory C fibres. 608 31

Combined retrograde axonal tracing with the fluorescent dye Fast Blue and fluoride-resistant acid phosphatase (FRAP) histochemistry revealed that the FRAP-containing sensory neurons project to both somatic and autonomic peripheral nerves. Furthermore, the combination of indirect immunohistochemistry after colchicine treatment and FRAP histochemistry showed that a population of FRAP-containing sensory neurons are also substance P, cholecystokinin or somatostatin positive.
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PMID:Peripheral projections and neuropeptide coexistence in a subpopulation of fluoride-resistant acid phosphatase reactive spinal primary sensory neurons. 609 69

(1) Capsaicin solution was applied for 15 min around a 1 cm length of sciatic nerve in the mid upper leg of adult rats. (2) Electron microscopic examinations of the nerve in the treated region after 14 days shows no signs of degeneration of either myelinated or unmyelinated fibres attributable to the capsaicin. (3) Fluoride resistant acid phosphatase FRAP disappears from the central terminals of the treated nerve by 7 days. (4) 1.5 mM capsaicin is sufficient to product a complete reduction of FRAP in the spinal cord. (5) The peptides substance P and cholecystokinin (CCK) are markedly depleted in the region of spinal cord terminations of the treated nerve at 14 days. (6) Substance P and CCk are not affected in spinal cord regions other than in the unmyelinated afferent terminal zone. Similarly neurotensin and neurophysin which are not present in afferent fibres are not influenced by capsaicin treatment of the sciatic. (7) It is concluded that there are chemical changes in the spinal cord terminals of fine afferents after local peripheral capsaicin.
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PMID:Effects of capsaicin applied locally to adult peripheral nerve. II. Anatomy and enzyme and peptide chemistry of peripheral nerve and spinal cord. 617 30

The distribution of fluoride-resistant acid phosphatase, substance P and somatostatin were investigated in the dorsal horn of the spinal cord and in dorsal root ganglia. In the dorsal horn, the distribution of fluoride-resistant acid phosphatase closely paralleled that of somatostatin and only partly overlapped with that of substance P. In sensory ganglia, none of the fluoride-resistant acid phosphatase-containing neurones contained either substance P or somatostatin. The results suggest the existence of a population of fluoride-resistant phosphatase-positive sensory neurones which is distinct from neurones containing either of these peptides.
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PMID:Fluoride-resistant acid phosphatase-containing neurones in dorsal root ganglia are separate from those containing substance P or somatostatin. 617 4

Capsaicin was applied locally to the sciatic or saphenous nerve, and the effects on axoplasmic transport, neurogenic plasma extravasation, and thermal pain were studied. Capsaicin (10 mg/ml) led to a complete block of axoplasmic transport of immunoreactive substance P (I-SP) and somatostatin (I-SRIF) in rat sciatic nerve without affecting the transport of noradrenaline or acetylcholinesterase. Inhibition of I-SP transport was also found in sciatic nerves of guinea-pig, cat and rabbit. In contrast, one or two weeks after systemic capsaicin treatment (125 mg/kg s.c.), orthograde transport of I-SP was the same in control and capsaicin-treated rats. After local capsaicin application to the sciatic nerve, a decrease of I-SP was found not only in skin and sciatic nerve distal to the site of application, but also in dorsal root ganglia, dorsal roots and the dorsal half of the spinal cord segments L 4-5. This was accompanied by a loss of acid phosphatase activity in the substantia gelatinosa supplied by sciatic nerve afferents. Plasma extravasation by mustard oil was reduced in the skin of the hind paw with a time course identical to the I-SP depletion. The response to noxious heat (hot plate test) was, however, abolished earlier. These results indicate that capsaicin applied to a peripheral nerve inhibits axoplasmic transport in sensory but not in adrenergic or cholinergic neurons, which leads to long-term biochemical and functional changes of the entire sensory neuron. In addition, capsaicin appears to inhibit impulse propagation in certain populations of sensory neurons.
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PMID:Capsaicin applied to peripheral nerve inhibits axoplasmic transport of substance P and somatostatin. 617 69

Vinblastine, a transport blocker, was applied locally to the sciatic nerve in rats. It was found to be a powerful neurotoxin with a dose-dependent action, destroying all afferents at doses of 5 X 10(-4)M, primarily C fibers at intermediate doses of 2.5 X 10(-4)M, and only at a critically low dose of 10(-4)M was a degeneration-free axon transport blockade, lasting for 4 to 5 days, produced. Such transport block failed to alter thermal responsiveness of the rats as measured behaviorally, by the flexor reflex, or by dorsal horn cell responses. It did, however, significantly reduce both the chemical sensitivity of the C afferents and their ability to produce neurogenic edema. This began 24 hr after treatment and lasted 4 to 5 days. Therefore, it is likely that these functions are dependent on the continuous transport of some compound to the axon terminals from the cell body. This low concentration of local vinblastine treatment also resulted in depletion of fluoride-resistant acid phosphatase from C fiber terminals in the dorsal horn of the spinal cord. Transmission from C fibers to second-order neurons in the spinal cord, however, was totally unaffected. Substance P levels in the spinal terminals was largely unaffected, although in 1 of 5 cases there was depletion. It appears, therefore, that some, but not all, retrograde changes in sensory neurons following peripheral nerve damage can be mimicked by blockade of axon transport. The effects following vinblastine treatment are compared to other peripheral nerve manipulations, such as cut, crush, and application of local capsaicin.
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PMID:Alterations in the structure, function, and chemistry of C fibers following local application of vinblastine to the sciatic nerve of the rat. 619 84

A gate control exists by which peripheral afferents and descending pathways can modulate sensory transmission. Evidence is presented that the mechanism may exist in the substantia gelatinosa laminae II and III. This area receives all known types of peripheral afferent from skin, from viscera and from high-threshold muscle afferents. The chemistry of the region is unique. Peripheral afferent terminals contain substance P, somatostatin, and fluoride-resistant acid phosphatase. Cells in the region contain enkephalin and GABA. At least three descending systems from the brainstem terminate in the area. The anatomical substrate exists by which cells in laminae II and III can receive afferents and descending axons and intrude onto cells of laminae I, IV, and V. Stimuli limited to the axons of laminae II and III cells in the Lissauer tract produce dorsal root potential and change the excitability of mono- and polysynaptic reflexes. They also change the excitability and receptive fields of cells in laminae IV and V. Recording from single units in laminae II and III reveals cells with many unusual properties not seen in the large dorsal horn cells. These unusual properties include small receptive fields, very prolonged responses to single stimuli, prolonged habituation, and shifting receptive fields. The action of the gate control shows it to be subtle and far beyond a simple control of overall excitability. Excitations and inhibitions are independently controlled. Different types of convergent afferent may be turned on and off. There are signs of both short-and long-lasting actions. It seems that a good case has been made for the cells of substantia gelatinosa taking part in the gate control mechanism.
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PMID:The role of substantia gelatinosa as a gate control. 624 35


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