INT127008
From wiki-pain
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Sentences Mentioned In
Key: | Protein | Mutation | Event | Anatomy | Negation | Speculation | Pain term | Disease term |
Using subcellular fractionation of proteins and cross-linking of membrane proteins we have observed that intracolonic capsaicin induced a 50% increase in NKCC1 in the plasma membrane of lumbosacral spinal cord 90 and 180 min after instillation, in parallel with a similar decrease in the cytosolic fraction. | |||||||||||||||
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-fiber input that is GABAergic in nature [13], 2) stroking allodynia following capsaicin injection into the hindpaw is absent in NKCC1 knockout mice [8], 3) spinal application of the NKCC1 blocker BUM inhibits intraplantar capsaicin-evoked, secondary mechanical allodynia in rats [10] and 4) a painful visceral stimulus increases dorsal horn NKCC1 phosphorylation and membrane trafficking [11], both of which are mechanisms known to increase NKCC1 activity and intracellular Cl- concentrations [1,26]. | |||||||||||||||
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We and others have proposed that GABAergic mechanisms may explain allodynia in inflamed conditions such that NKCC1 activity increases leading to a large depolarization in C-fibers, causing spiking, in response to A? | |||||||||||||||
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Moreover, they suggest that endogenous TRPV1 agonists, released in the CNS in painful conditions, might stimulate TRPV1 receptors on primary afferents that, in turn, play a role in increasing NKCC1 activity leading to allodynia.
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leading to an increase in NKCC1 activity causing touch evoked pain. | |||||||||||||||
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Finally, intracolonic capsaicin injection stimulates a rapid and transient increase in spinal phosphorylated NKCC1 and a long lasting increase in trafficking of NKCC1 protein to the plasma membrane [11]. | |||||||||||||||
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