Figure 1.

pNKCC1 expression is increased after nerve injury in DRGs. A, B, Representative WBs and quantification of NKCC1 and pNKCC1 expression changes at early time points (3, 8, and 16 DPI) in injured (black) and uninjured (white) samples. D, E, Increased expression of pNKCC1 after injury is prevented by bumetanide administration (30 mg/kg; vehicle vs naive, **p < 0.01; vehicle vs bumetanide ***p < 0.001) in the ipsilateral (ipsi) and contralateral (contra) side of the injured paw. WB quantification is shown at the final time point of bumetanide administration (16 DPI). C, F, Confocal images show the increased localization of NKCC1 in the membrane of DRG neurons, labeled with NF200 structural marker, in injured animals and its prevention by bumetanide administration. Arrowheads point membrane-bound or cytoplasmatic localization of NKCC1 in injured (C) or vehicle and bumetanide treated groups (F). Scale bar, 100 μm. Inset boxes show detailed neurons labeled with NKCC1 (scale bar, 10 μm). Data are presented as the mean ± SEM. Ipsi, Ipsilateral; Contra, contralateral.