INT100115
From wiki-pain
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Sentences Mentioned In
Key: | Protein | Mutation | Event | Anatomy | Negation | Speculation | Pain term | Disease term |
We also used a monoclonal antibody to the NKCC1 form of the Na-K-2Cl cotransporter to show that NKCC1 is expressed in optic nerves as shown in Western blotting and is colocalized in GFAP immunopositive astrocytes. | |||||||||||||||
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Cation chloride cotransporters, K(+)-Cl(-) cotransporter 2 (KCC2) and Na(+)-K(+)-Cl(-) cotransporter 1 (NKCC1) are reported to be expressed in the neurons in the spinal cord and regulate intracellular Cl(-) concentration. | |||||||||||||||
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While the expression of NKCC1 in DRG neurons is well documented (e.g. [13] and references therein), there are conflicting results about the expression of KCC2. | |||||||||||||||
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For DRG neurons, the expression of NKCC1 is well documented [13,22], while the expression of KCC2 is controversial [23,24]. | |||||||||||||||
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While the changes in NKCC1 and KCC2 expression are consistent with increased Cl- accumulation, the time course of the expression changes lags behind the rise in [Cl-]i. | |||||||||||||||
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0.001) above control, while the total expression level of NKCC1 showed no response (Fig. 3). | |||||||||||||||
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We investigated the expression of potassium-chloride co-transporter 2 (KCC2) and sodium-potassium-chloride co-transporter 1 (NKCC1) in the rat spinal cord after peripheral inflammation induced by complete Freund's adjuvant (CFA) injection. | |||||||||||||||
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Our results suggest that the expression of KCC2, but not that of NKCC1, was significantly reduced in CFA-injected rats. | |||||||||||||||
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Expression of NKCC1 and KCC2 following SCI | |||||||||||||||
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A low level of NKCC1 protein was expressed in the spinal cord tissue at baseline (Figure 2A). ? | |||||||||||||||
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These results imply that altered NKCC1 and KCC2 expression may lead to GABAergic derangement and contribute to the induction and maintenance of the chronic neuropathic pain following SCI. | |||||||||||||||
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This data indicate a significant increase in the expression of NKCC1 and, conversely, a decrease in KCC2 expression at the epicenter on day 14 post-SCI (prior to the chronic phase of post-SCI neuropathic hyperalgesia). | |||||||||||||||
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Both NKCC1 and KCC2 are expressed in spinal cords and function to regulate intracellular Cl- concentration. | |||||||||||||||
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The effect of the mediators is consistent with increased Cl- accumulation, as NKCC1 expression is enhanced, while KCC2 expression is attenuated.
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These data demonstrate that NKCC1 and KCC2 expression levels remain unchanged over 2 hr of treatment with inflammatory mediators. | |||||||||||||||
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The antisera directed against NKCC1 (C-14 antibody) and p-NKCC1 showed a virtually perfect match in the DRG sections (Fig. 4A) indicating that both non-phosphorylated and phosphorylated forms of NKCC1 are present in most neurons. | |||||||||||||||
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We, therefore, investigated expression changes of KCC2 and NKCC1 in the spinal dorsal horn of the rat after the intraplantar injection of formalin as an acute nociceptive stimulus. | |||||||||||||||
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NKCC1 is very weakly expressed in adult dorsal horn neurons [29,30] but is the dominant cation-chloride co-transporter in primary afferents [31], and thus NKCC1 leads to GABA exerting a depolarizing, albeit inhibitory, action on sensory terminals. | |||||||||||||||
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Our objective was to monitor changes of the intracellular Cl- concentration as well as changes in expression of NKCC1 and KCC2 in the presence of inflammatory mediators. | |||||||||||||||
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We find that inflammatory mediators cause an increase of Cl- levels in DRG neurons which correlates with enhanced NKCC1 expression and decreased KCC2 expression.
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General Comments
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