Peripheral Neuropathy With Diabetic Co-Morbidities
STZ is commonly used to induce type I diabetes and diabetes related complications including diabetic peripheral neuropathy. There are multiple theories on the mechanism that involves peripheral neuropathy following STZ. Some of the mechanisms suggested are related to the hyperglycemic state of the rats suggesting that following the hyperglycemia, nerve endings are damaged either through an inflammatory process or interfering with blood supply (ischemia of the micro vessels). However, vast studies are also suggesting a mechanism of neuronal damage that occurs following STZ but it is unrelated to the hyperglycemic state of the animals. These studies suggest direct damage to the nerves. For example, reactive oxygen species (ROS) mediate elevation of TRPV1 in neurons and the DRG is expsed to STZ in vitro. Therefore, this model involves direct changes in the nerves that are not related to the inflammatory process.
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Longitudinal Von Frey (tactile allodynia) measurements in rat STZ diabetic neuropathy model