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Fig. 1 Acute hyperglycemia induces degeneration of the perineurial structure ensheathing the motor nerves. (A) A schematic outlining hyperglycemia-inducing treatment schedule. (B) Following the schedule of treatment described in (A), there was a significant increase in whole-body glucose levels in Tx12 fish compared to C12 fish, ****P < .0001. (C) Schematic representation of the orientations of lateral and coronal views of peripheral motor nerves. (D and E) Lateral view of C12 and Tx12 Tg(nkx2.2a:mEGFP);Tg(NBT:DsRed) zebrafish. Ensheathment of peripheral motor axons (red) by perineurial glia (green) appeared continuous along the length of the axons in C12 fish (D, asterisk). The perineurium in Tx12 fish often appeared disassociated from axons (E, arrow), absent (E, asterisk), or associated with debris (E, arrowhead). (F) The percentage of perineurial-ensheathed motor axons was significantly lower in Tx12 fish compared to C12 fish, ****P < .0001. (G) The length of perineurial-ensheathment was also significantly lower in Tx12 fish than C12 fish, ****P < .0001. (H and I) Representative images of C12 and Tx12 Tg(nkx2.2a:mEGFP) zebrafish antibody labeled against zonula occludens-1 (ZO-1, red). In C12 fish, ZO-1+ tight junctions were present along the length of the entire perineurium (H″, arrow), whereas in Tx12 fish, ZO-1+ tight junctions were diminished and discontinuous along the perineurium (I″, arrow). (J) ZO-1+ fluorescent intensity (standardized to nkx2.2a) was diminished in Tx12 fish compared to C12 fish, ****P < .0001 (au, arbitrary units). All values are means ± SEM. Scale bars = 50 μm.