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 influence of the serotonin (5-HT) system on the release of immunoreactive substance P after electrical stimulation of the lower incisor pulp was examined by perfusion of the superficial layers of the subnucleus caudalis of the brain stem trigeminal sensory nuclear complex of rabbits in situ. Increased release of immunoreactive substance P was observed after electrical stimulation of the pulp at 40 V. Stimulation of the nucleus raphe magnus significantly increased the release of 5-HT and completely inhibited the release of immunoreactive substance P, evoked by stimulation of the tooth pulp. Local application of 5-HT (10(-6) M) inhibited the release of immunoreactive substance P induced by stimulation and this inhibition was antagonized by methysergide (10(-4) M) applied concomitantly to the superficial layers of the trigeminal nucleus. These results suggest a functional interaction between substance P and 5-HT in the superficial layers of the trigeminal nucleus for regulation of transmission of dental pain.
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PMID:Serotonin inhibits release of substance P evoked by tooth pulp stimulation in trigeminal nucleus caudalis in rabbits. 171 Jul 94

The modulation of dental pain transmission at the subnucleus caudalis of the trigeminal sensory nuclear complex (SpVc) was investigated in rabbits in vivo. The superficial layers of SpVc were perfused with artificial cerebrospinal fluid using a push-pull cannula system. Immunoreactive substance P (SP) released into the perfusates following electrical stimulation of the lower incisor pulp was measured. The obtained results were as follows. 1. An increase in the release of SP and [Met5]-enkephalin was observed by the electrical stimulation with 40 V. 2. The increase of SP release following electrical stimulation was inhibited by systemic administration of morphine (10 mg/kg i.v.) or local application of morphine (10(-6) M) to SpVc. The stimulus-evoked SP release was also inhibited by local application of [D-Ala2, Met5]-enkephalinamide (an analog of [Met5]-enkephalin; 10(-4) M). 3. Spontaneous release of serotonin (5-HT) into the perfusates was observed, while that of norepinephrine was not. Tooth pulp stimulation tended to increase the level of 5-HT. Systemic administration of morphine (10 mg/kg i.v.) and electrical stimulation of the nucleus raphe magnus (NRM) significantly enhanced the release of 5-HT. 4. The release of SP evoked by tooth pulp stimulation was inhibited by local application of 5-HT (10(-6)M) and electrical stimulation of NRM. These results suggest that there are two modulatory systems controlling the delivery of the ascending sensory message at the superficial layers of SpVc. One is an intrinsic mechanism associated with the segmental enkephalinergic system, the other is a descending monoaminergic system originating in NRM. It is also suggested that these two systems play an important role in producing the analgesic effect of morphine.
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PMID:[Mechanism of the modulation of pain transmission at the subnucleus caudalis of the trigeminal sensory nuclear complex in rabbits]. 172 94

Perfusates were taken from the superficial layers of the subnucleus caudalis of the trigeminal sensory nuclear complex (SpVc), the first relay station of dental pain, with a push-pull cannula system and were assayed for endogenous serotonin (5-HT) and catecholamines by high-pressure liquid chromatography with an electrochemical detection. Spontaneous release of 5-HT and epinephrine was observed, while that of norepinephrine was not. Tooth pulp stimulation (ST) tended to increase the level of 5-HT in the perfusates. Pretreatment with morphine at a dose of 10 mg/kg (i.v.) significantly enhanced the release of 5-HT. However, there was no significant difference in morphine effect on the 5-HT level between stimulated and non-stimulated animals. Systemic administration of morphine (10 mg/kg i.v.) completely inhibited the release of immunoreactive substance P from the superficial layers of SpVc evoked by ST, and this inhibition was antagonized by local application of methysergide (10(-4) M). These results suggest that in the superficial layers of SpVc, morphine may primarily activate the descending 5-HT pathway which serves to modulate dental pain transmission.
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PMID:Involvement of descending monoaminergic systems in the transmission of dental pain in the trigeminal nucleus caudalis of the rabbit. 230 14

The superficial layer in subnucleus caudalis of the brain-stem trigeminal sensory nuclear complex (SpVc) in the rabbit was perfused with artificial cerebrospinal fluid using a push-pull perfusion cannula system. Immunoreactive substance P (iSP) and [Met5]enkephalin (iME) released into the perfusates following electrical stimulation of the lower incisor pulp were measured. An increase in the release of iSP and iME lasting for 1 h or more was observed following electrical stimulation with 40 V. The increase in iSP release depended on the intensity of stimulation. Systemic morphine (10 mg/kg i.v.) completely inhibited the stimulus-evoked iSP release and this inhibition was antagonized by pretreatment with naloxone (5 mg/kg i.v.). The stimulus-evoked iSP release was also inhibited by local application of morphine (10(-6) M) or the opioid peptide [D-Ala2,Met5]enkephalinamide (10(-4) M). However, the local application of naloxone (5 X 10(-7) M) only partially antagonized the inhibitory effects of locally applied morphine and the opioid peptide. These results suggest that there is a functional interaction between SP and enkephalin systems in the superficial layer of SpVc for the regulation of dental pain transmission.
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PMID:Effects of opioids and opioid peptide on the release of substance P-like material induced by tooth pulp stimulation in the trigeminal nucleus caudalis of the rabbit. 243 Aug 13

The increase of knowledges in the field of endorphines and other peptides causes new aspects of development and transmission of dental pain. Methionin-enkephalin (ME) and substance P (SP) are found also in the dental pulp and the dentine. The concentration of SP is higher in the pulp, than in some other tissues. The concentration of both, ME and SP, in the endodont is different with respect to different functional situations, e.g. it is lower in case of pain. We suppose, there is a peptiderg reception and transmission of pain in dentine. Interaction with this new system opens new ways for opposing pulpal pain.
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PMID:[The significance of endogenous peptides for dental pulp pain]. 247 94

Substance P-like and enkephalin-like immunoreactive nerve fibers were observed in the human tooth pulp. Immunoreactivity for substance P could be demonstrated in thin, beaded nerve fibers and glomerular-type nerve structures both in the center and in more peripheral parts of the tooth pulp. Substance P-like nerve fibers predominated in the center of the pulp substance, while a thicker type of enkephalin-like nerve fibers were more commonly seen at the periphery of the pulp. Controls exhibited no immunoreactivity for either neuropeptide. It is tentatively suggested that a dual innervation by substance P-like fibers and enkephalin-like nerve fibers may be involved in the mediation of toothache in man.
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PMID:Peptidergic nerves in human tooth pulp. 620 53

Dental pulp is a soft mesenchymal tissue densely innervated by afferent (sensory) fibers, sympathetic fibers, and parasympathetic fibers. This complexity in pulp innervation has motivated numerous investigations regarding how these 3 major neuronal systems regulate pulp physiology and pathology. Most of this research is focused on neuropeptides and their role in regulating pulpal blood flow and the development of neurogenic inflammation. These neuropeptides include substance P, calcitonin gene-related peptide, neurokinin A, neuropeptide Y, and vasoactive intestinal polypeptide among others. The purpose of this article is to review recent advances in neuropeptide research on dental pulp, including their role in pulp physiology, their release in response to common dental procedures, and their plasticity in response to extensive pulp and dentin injuries. Special attention will be given to neuropeptide interactions with pulp and immune cells via receptors, including studies regarding receptor identification, characterization, mechanisms of action, and their effects in the development of neurogenic inflammation leading to pulp necrosis. Their role in the growth and expansion of periapical lesions will also be discussed. Because centrally released neuropeptides are involved in the development of dental pain, the pain mechanisms of the pulpodentin complex and the effectiveness of present and future pharmacologic therapies for the control of dental pain will be reviewed, including receptor antagonists currently under research. Finally, potential clinical therapies will be proposed, particularly aimed to manipulate neuropeptide expression or blocking their receptors, to modulate a variety of biologic mechanisms, which preliminary results have shown optimistic results.
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PMID:Neuropeptides in dental pulp: the silent protagonists. 1857 Sep 80

One minute downward pressure on the tip of any one of the front 3 teeth (1st incisor, 2nd incisor, and canine) at the right and left sides of the upper and lower jaw by a wooden toothpick induced temporary disappearance (20 min approximately 4 hours) of abnormally increased pain parameters (pain grading, Substance P, & TXB2), and cancer parameters (Telomere, Integrin alpha5beta1, Oncogene C-fos Ab2, etc. of Astrocytoma, Glioblastoma, squamous cell carcinoma of esophagus, adenocarcinoma of lung, breast cancer, adenocarcinoma of colon, prostate cancer). The effect included temporary disappearance of headache, toothache, chest and abdominal pain, and backache, often with improved memory & concentration. Since these beneficial changes resembled the effects of giving one optimal dose of DHEA, increase of DHEA was measured. Above mechanical stimulation of one of these front teeth increased abnormally reduced DHEA levels of less than 10 ng to norm1 100 approximately 130 ng BDORT units and normal cell (NC) telomeres from markedly reduced values to near normal values, and improved acetylcholine in the Hippocampus. Large organ representation areas for the Adrenal gland & Hippocampus may exist at these front teeth. This method can be used for emergency pain control and can explain the beneficial effect of bruxism and tooth brushing, through the increase of DHEA levels and activities of the Hippocampus by increasing Acetylcholine. Increasing NC telomere to optimally high level resulted in disappearance of pain and improvement or significant reduction of malignant tumor. Repeated daily press needle stimulation of True ST. 36 increased NC telomere 450-700 ng BDORT units. One optimal dose of DHEA increased NC telomere 525 ng DBORT units and eliminated the pain and abnormally increased cancer parameters; effect of one optimal dose lasted 0.5-11 months. One optimal dose of Boswellia Serrata or Astragalus not only increased NC telomere 650 ng BDORT units, eliminating pain and cancer parameters, but also reduced the size of the Astrocytoma grade I by 10-20% and the Glioblastoma by 15-90% in less than 2-6 months in some patients, as long as high NC telomere is maintained.
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PMID:Temporary anti-cancer & anti-pain effects of mechanical stimulation of any one of 3 front teeth (1st incisor, 2nd incisor, & canine) of right & left side of upper & lower jaws and their possible mechanism, & relatively long term disappearance of pain & cancer parameters by one optimal dose of DHEA, Astragalus, Boswellia Serrata, often with press needle stimulation of True ST. 36. 2034 85

Current evidence supports the central role of neuropeptides in the molecular mechanisms underlying dental pain. In particular, substance P, a neuropeptide produced in neuron cell bodies localised in dorsal root and trigeminal ganglia, contributes to the transmission and maintenance of noxious stimuli and inflammatory processes. The major role of substance P in the onset of dental pain and inflammation is increasingly being recognised. Well-grounded experimental and clinical observations have documented an increase in substance P concentration in patients affected by caries, pulpitis, or granulomas and in those undergoing standard orthodontic or orthodontic/dental care procedures. This paper focuses on the role of substance P in the induction and maintenance of inflammation and dental pain, in order to define future lines of research for the evaluation of therapeutic strategies aimed at modulating the complex effects of this mediator in oral tissues.
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PMID:Peripheral mechanisms of dental pain: the role of substance P. 2247 2

Information on the frequency and spatial distribution of axonal varicosities associated with release of neurotransmitters in the dental pulp is important to help elucidate the peripheral mechanisms of dental pain, mediated by myelinated versus unmyelinated fibers. For this, we investigated the distribution of axonal varicosities in the human dental pulp using light- and electron-microscopic immunohistochemistry for the vesicular glutamate transporter 2 (VGLUT2), which is involved in the glutamatergic transmission, and syntaxin-1 and synaptosomal nerve-associated protein 25 (SNAP-25), combined with parvalbumin (PV), which is expressed mostly in myelinated axons, and substance P (SP) and calcitonin gene-related peptide (CGRP), which are expressed mostly in unmyelinated axons. We found that the varicosities of the SP- and CGRP-immunopositive (+) axons were uniformly distributed throughout the dental pulp, whereas those of PV+ axons were only dense in the peripheral pulp, and that the expression of PV, VGLUT2, syntaxin-1, SNAP-25, SP and CGRP was significantly higher in the varicosities than in the axonal segments between them. These findings are consistent with the release of glutamate and neuropeptides by axonal varicosities of SP+ and CGRP+ unmyelinated fibers, involved in pulpal pain throughout the human dental pulp, and by varicosities of PV+ fibers, arising from parent myelinated fibers, and involved in dentin sensitivity primarily in the peripheral pulp.
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PMID:Parvalbumin-, substance P- and calcitonin gene-related peptide-immunopositive axons in the human dental pulp differ in their distribution of varicosities. 3260 38


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