Diabetic α1H−/− mice do not develop early hyperalgesia and are resistant to the effects of ECN in tests of mechanical and
thermal sensitivity. A: When 200 mg/kg STZ was administrated intraperitoneally to α1H+/+ mice (circles) and α1H−/− mice (squares), PWLs for the
first 4 weeks post-STZ were significantly different between the two groups (#P < 0.001). Compared with their initial baselines, only α1H+/+ developed heat hypersensitivity (*P < 0.01). Both groups developed hyperglycemia to a similar extent (see insert) with blood glucose greater than initial day
0 values (*P < 0.001) (n = 5 α1H−/− mice per group; n = 7 α1H+/+ mice per group). B: When 25 mg/kg of ECN was administered intraperitoneally to diabetic α1H+/+ mice (1–2 weeks after STZ treatment), there was,
between 60 and 120 min after ECN injection, a significant increase in PWLs in both right (●) and left paws (○) as compared
with PWLs at 0 min (immediately before injection) (*P < 0.001). C: The same dose of ECN had no effect on thermal sensitivity in diabetic α1H−/− mice (also 1–2 weeks after STZ) throughout
the testing period (n = 5 α1H−/− mice per group; n = 6 α1H+/+ mice per group). D and E: When mechanical sensitivity was tested at 90 to 120 min after injection of 25 mg/kg of ECN, there was a significant decrease
in PWRs in diabetic α1H +/+ mice as compared with those at 0 min (panel D) (*P < 0.001) but no effect on PWRs of diabetic α1H−/− mice (E) (n = 5 α1H−/− mice per group; n = 6 α1H+/+ mice per group).