The effects of type 1 diabetes on the mechanoreflex in rats
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Mechanical allodynia is present as early as four days in streptozotocin (STZ) induced type 1 diabetes mellitus (T1DM) in rats. This is thought to occur through mechanisms affecting the same thin fiber afferents that evoke the mechanoreflex. In this study, the purpose was to determine the effects of T1DM on the mechanoreflex. We injected (i.p.) 50 mg/kg of Streptozotocin (STZ) or the vehicle (CTL) in both sexes and waited 1wk (STZ: BW=251.2±11.47g, glucose=468.1±23.18mg/dL, HbA1C=6.09±02%; CTL: BW=351.5±21.01g, glucose=176.3±10.94mg/dL, HbA1C=4.23±0.12%). In unanesthetized decerebrate rats, we stretched the Achilles tendon for 30s and measured the pressor and cardioaccelerator responses. We then compared the pressor and cardioaccelerator responses to tendon stretch before and after inhibition of Piezo 1 and 2 channels. Inhibition was done by injecting GsMTx-4 (10μg/100μl), a selective mechano- gated Piezo channel inhibitor, into the arterial supply of the hindlimb muscles in rats. We found that the pressor (STZ: ΔMAP=42.1±8.3 mmHg, n=9; CTL: ΔMAP=18.7±4.0 mmHg, n=6; p<0.05) but not the cardioaccelerator (STZ: ΔHR=13.6±3.7 bpm, n=9; CTL: ΔHR=9.7±2.7 bpm, n=6; p>0.05) responses to tendon stretch were exaggerated 1wk after injecting STZ. Furthermore, GsMTx-4 appears to attenuate the pressor (before GsMTx-4: ΔMAP=65.33±4.98 mmHg; after GsMTx-4: ΔMAP=46±4.16 mmHg, n=3; p<0.05) but not cardioaccelerator (before GsMTx-4: ΔHR=16.67±4.18 bpm; after GsMTx-4: ΔHR=13.33±6.77 bpm, n=3; p>0.05) responses to tendon stretch in rats 1wk after STZ injection. The developed tensions from tendon stretch were similar within each comparison. We conclude that the mechanoreflex is augmented in the early stage of T1DM and that Piezo channels likely play a role in this response.