Diabetes was induced in three mouse lines: C57BL/6 mice (Jackson Laboratory, Stock#: 000664, RRID:IMSR_JAX:000664), NG2-DsRed mice (Jackson Laboratory, Tg(Cspg4-DsRed.T1)1Akik/J, Stock#: 008241, RRID:IMSR_JAX:008241) and NG2-Cre-GCamp6f, generated by crossing FVB-lfi208Tg(Cspg4-cre)1Akik/J (Jackson Laboratory, Stock#: 008533, RRID:IMSR_JAX 008533) with Ai95(RCL-GCaMP6f)-D loxP (Jackson Laboratory, Stock#: 024195, RRID:IMSR_JAX 024195). Breeding pairs negative for the rd1 mutation were used to produce animals for this study. We used the STZ diabetic mouse model57 (link). Male mice aged 6–8 weeks were fasted for 4 h prior to the injections. The animals were injected intraperitoneally on 5 consecutive days with 50 mg/kg STZ (Sigma-Aldrich, S0130) freshly dissolved in a citrate buffer (pH 4.5). Control animals received a citrate buffer injection without STZ. In our STZ mouse model of diabetes, the levels of blood glucose reached maximum elevation 1 month after STZ injection and remained elevated. The diabetes was defined by non-fasting blood glucose >300 mg/dL verified 1 month after the last STZ injection and confirmed on the day of the experiment.
Free full text: Click here