Abstract

Earlier, considerable prolongation of the depolarization-induced Ca2+ transients was demonstrated in primary sensory neurons of rats with streptozotocin (STZ)-induced diabetes mellitus. To analyze the nature of this effect, we examine possible changes in the characteristics of voltage-operated calcium channels. Neither the amplitude of Ca2+ currents provided by both high- and low-voltage activated calcium channels nor the respective current densities significantly changed within the early stages of diabetes mellitus. In rats treated with nimodipine, also no significant changes in the calcium channel activity were observed. Only in the case of a decrease in the external calcium concentration was some drop in the Ca2+ current amplitude observed. We conclude that within the early stages of diabetes mellitus there are no significant modifications in the structure of the membrane of primary sensory neurons manifested in the expression of Ca2+ channels, which might be responsible for the observed rapidly occurring changes in calcium signalling, cytosolic Ca2+ accumulation, and synaptic plasticity.

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