INT4850
From wiki-pain
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Sentences Mentioned In
Key: | Protein | Mutation | Event | Anatomy | Negation | Speculation | Pain term | Disease term |
Subsequent to its release, substance P binds to neurokinin-1 (NK-1) receptors on the surface of effector cells and, in addition to being a mediator of pain, it plays an important role in many inflammatory states including asthma, immune-complex-mediated lung injury, experimental arthritis, and inflammatory bowel disease. | |||||||||||||||
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We conclude that 1) substance P stimulates extravasation in the gastrointestinal tract and pancreas of mice by interacting with the NK1 receptors, and 2) capsaicin and bradykinin induce plasma extravasation by stimulating tachykinin release from sensory nerves. | |||||||||||||||
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These data suggest that the N-terminus of SP is responsible for down-regulation of NK-1 binding. | |||||||||||||||
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Injected intrathecally, substance P (SP) down-regulates neurokinin-1 (NK-1) binding in the spinal cord and desensitizes rats to the behavioral effect of SP. | |||||||||||||||
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An N-terminal fragment of substance P, substance P(1-7), down-regulates neurokinin-1 binding in the mouse spinal cord. | |||||||||||||||
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Injected intrathecally, substance P (SP) down-regulates neurokinin-1 (NK-1) binding in the spinal cord and desensitizes rats to the behavioral effect of SP. | |||||||||||||||
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The goal of this study was to assess the abilities of N- and C-terminal fragments of SP to down-regulate NK-1 binding. | |||||||||||||||
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As SP(5-11) did not down-regulate NK-1 binding, activation of NK-1 sites does not appear necessary or sufficient for down-regulation of SP binding. | |||||||||||||||
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Subsequent to its release, substance P binds to neurokinin-1 (NK-1) receptors on the surface of effector cells and, in addition to being a mediator of pain, it plays an important role in many inflammatory states including asthma, immune-complex-mediated lung injury, experimental arthritis, and inflammatory bowel disease. | |||||||||||||||
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The present investigation was initiated to determine whether N-terminal fragments interact at binding sites distinct from the neurokinin-1 (NK-1) receptor where the C-terminal sequence of SP binds with high affinity, and distinct from mu-opiate receptors, where we have previously shown the N-terminal sequence of SP to interact. | |||||||||||||||
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Based on this report, the present study was conducted to further investigate the direct functional interaction between supraspinal tachykinin (r/m HK-1) and opioid systems. | |||||||||||||||
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At the age of 2 to 4 months, binding of 125I-labelled Tyr8-substance P to synaptic vesicles prepared from different regions of the nervous system was examined. | |||||||||||||||
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In contrast, SP(1-7), in spite of its inability to interact with NK-1 sites, did down-regulate SP binding, suggesting an indirect mechanism dissociated from NK-1 receptors. | |||||||||||||||
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Substance P and bradykinin stimulated extravasation from postcapillary venules in the stomach, small and large intestine, pancreas, urinary bladder, trachea, and skin by two- to sevenfold by interacting with NK1 and B2 receptors, respectively. | |||||||||||||||
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The present investigation was initiated to determine whether N-terminal fragments interact at binding sites distinct from the neurokinin-1 (NK-1) receptor where the C-terminal sequence of SP binds with high affinity, and distinct from mu-opiate receptors, where we have previously shown the N-terminal sequence of SP to interact. | |||||||||||||||
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To test these compounds preclinically, gerbils have become one of the preferred species in that they demonstrate close NK1 receptor homology with humans and bind NK1 antagonists with higher affinity than rats and mice. | |||||||||||||||
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Interactions between serotonin and substance P in the spinal regulation of nociception. | |||||||||||||||
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Interactions between 5-hydroxytryptamine (5-HT) and substance P (SP) in the mouse spinal cord were investigated using the tail-flick test and the behavioral response evoked by intrathecal (i.th.) | |||||||||||||||
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These findings indicate a functional interaction between substance P and 5-HT in the modulation of sensory input at the spinal level. | |||||||||||||||
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Besides SP, peptide hormones such as hemokinin can also bind and activate NK1 at sites of chronic inflammation [44]. | |||||||||||||||
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General Comments
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