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- W2106204024 abstract "Background: ATP-sensitive potassium (K ATP ) channels in neurons mediate neuroprotection, they regulate membrane excitability, and they control neurotransmitter release. Because loss of DRG neuronal K ATP currents is involved in the pathophysiology of pain after peripheral nerve injury, we characterized the distribution of the K ATP channel subunits in rat DRG, and determined their alterations by painful axotomy using RT-PCR, immunohistochemistry and electron microscopy. Results: PCR demonstrated Kir6.1, Kir6.2, SUR1 and SUR2 transcripts in control DRG neurons. Protein expression for all but Kir6.1 was confirmed by Western blots and immunohistochemistry. Immunostaining of these subunits was identified by fluorescent and confocal microscopy in plasmalemmal and nuclear membranes, in the cytosol, along the peripheral fibers, and in satellite glial cells. Kir6.2 co-localized with SUR1 subunits. Kir6.2, SUR1, and SUR2 subunits were identified in neuronal subpopulations, categorized by positive or negative NF200 or CGRP staining. K ATP current recorded in excised patches was blocked by glybenclamide, but preincubation with antibody against SUR1 abolished this blocking effect of glybenclamide, confirming that the antibody targets the SUR1 protein in the neuronal plasmalemmal membrane. In the myelinated nerve fibers we observed anti-SUR1 immunostaining in regularly spaced funneled-shaped structures. These structures were identified by electron microscopy as Schmidt-Lanterman incisures (SLI) formed by the Schwann cells. Immunostaining against SUR1 and Kir6.2 colocalized with anti-Caspr at paranodal sites. DRG excised from rats made hyperalgesic by spinal nerve ligation exhibited similar staining against Kir6.2, SUR1 or SUR2 as DRG from controls, but showed decreased prevalence of SUR1 immunofluorescent NF200 positive neurons. In DRG and dorsal roots proximal to axotomy SLI were smaller and showed decreased SUR1 immunofluorescence. Conclusions: We identified Kir6.2/SUR1 and Kir6.2/SUR2 K ATP channels in rat DRG neuronal somata, peripheral nerve fibers, and glial satellite and Schwann cells, in both normal state and after painful nerve injury. This is the first report of K ATP channels in paranodal sites adjacent to nodes of Ranvier and in the SLI of the Schwann cells. After painful axotomy K ATP channels are downregulated in large, myelinated somata and also in SLI, which are also of smaller size compared to controls. Because K ATP channels may have diverse functional roles in neurons and glia, further studies are needed to explore the potential of K ATP channels as targets of therapies against neuropathic pain and neurodegeneration." @default.
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- W2106204024 date "2010-01-01" @default.
- W2106204024 modified "2023-10-17" @default.
- W2106204024 title "K<sub>ATP</sub> Channel Subunits in Rat Dorsal Root Ganglia: Alterations by Painful Axotomy" @default.
- W2106204024 cites W1512324842 @default.
- W2106204024 cites W1816134939 @default.
- W2106204024 cites W1844683293 @default.
- W2106204024 cites W1917747879 @default.
- W2106204024 cites W1965679116 @default.
- W2106204024 cites W1965866432 @default.
- W2106204024 cites W1966721481 @default.
- W2106204024 cites W1969166255 @default.
- W2106204024 cites W1970911947 @default.
- W2106204024 cites W1971542798 @default.
- W2106204024 cites W1975898528 @default.
- W2106204024 cites W1984789478 @default.
- W2106204024 cites W1985167281 @default.
- W2106204024 cites W1988472754 @default.
- W2106204024 cites W1990210584 @default.
- W2106204024 cites W1994463799 @default.
- W2106204024 cites W2005276070 @default.
- W2106204024 cites W2006424917 @default.
- W2106204024 cites W2008390218 @default.
- W2106204024 cites W2010383551 @default.
- W2106204024 cites W2028641524 @default.
- W2106204024 cites W2029335288 @default.
- W2106204024 cites W2030560521 @default.
- W2106204024 cites W2032302528 @default.
- W2106204024 cites W2033349405 @default.
- W2106204024 cites W2039969107 @default.
- W2106204024 cites W2040681679 @default.
- W2106204024 cites W2041817283 @default.
- W2106204024 cites W2042847772 @default.
- W2106204024 cites W2053578197 @default.
- W2106204024 cites W2056839311 @default.
- W2106204024 cites W2056902643 @default.
- W2106204024 cites W2059892947 @default.
- W2106204024 cites W2067581172 @default.
- W2106204024 cites W2074290857 @default.
- W2106204024 cites W2077392459 @default.
- W2106204024 cites W2080366678 @default.
- W2106204024 cites W2080606376 @default.
- W2106204024 cites W2082083680 @default.
- W2106204024 cites W2085213849 @default.
- W2106204024 cites W2087910402 @default.
- W2106204024 cites W2089221620 @default.
- W2106204024 cites W2091883621 @default.
- W2106204024 cites W2092404026 @default.
- W2106204024 cites W2121104497 @default.
- W2106204024 cites W2121962823 @default.
- W2106204024 cites W2127552748 @default.
- W2106204024 cites W2129155410 @default.
- W2106204024 cites W2144632824 @default.
- W2106204024 cites W2150674406 @default.
- W2106204024 cites W2150796852 @default.
- W2106204024 cites W2152043216 @default.
- W2106204024 cites W2160723322 @default.
- W2106204024 cites W2161945723 @default.
- W2106204024 cites W2166610424 @default.
- W2106204024 cites W2166660871 @default.
- W2106204024 cites W2169917556 @default.
- W2106204024 cites W2331570632 @default.
- W2106204024 doi "https://doi.org/10.1186/1744-8069-6-6" @default.
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