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The effect of insulin on the response to long-term high-frequency stimulation (HFS = 143 Hz for 20 min) was studied in mixed tail nerves of acute streptozotocin-induced diabetic rats. In consecutive tests, untreated diabetic rats showed a significant decrease in nerve conduction velocity (NCV) and peak-to-peak amplitude (P-Pamp) and the depression of the P-Pamp during HFS was augmented. In contrast, NCV and P-Pamp in the insulin-treated rats were unchanged from the prediabetic state, but the depression of the P-Pamp during HFS reached the same degree as in untreated rats. This implies that although insulin treatment of acute experimental diabetes is able to preserve a normal NCV and P-Pamp in the resting state, it is unable to preserve normal nerve function under stress produced by HFS. Monitoring of the axon membrane functional capacity may have clinical implications in the control of peripheral neuropathies.
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Andersen et al. (1994) studied this question.
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