Distal symmetric neuropathy is a common syndrome originating during many forms of general pathology. Its development is to a large extent connected with alterations of synaptic transmission between primary and secondary nociceptive neurons. An important feature of changes in the signaling machinery in these neurons was shown to be a substantial prolongation of depolarization-induced intracellular calcium transients. Possible mitochondrial role in such changes was proposed.Alterations in the calcium accumulating function of mitochondria appearing under streptozotocine-induced diabetes were studied in acutely isolated nociceptive DRG neurons from rats. Cytoplasmic calcium concentration ([Ca2+]i) was recorded using indo-1/AM microfluorimetry; Ca2+ uptake by mitochondria has been calculated by subtraction of depolarization-induced [Ca2+]i transients measured after application of mitochondrial protonophore CCCP from [Ca2+]i transients in the same cell before such application. In such way a quantitative analysis of mitochondrial modification of the amplitude and time-course of depolarization-trigged calcium signals was made. It was shown that diabetes results in a very significant (24 %) decrease in the effectiveness of mitochondrial calcium uptake in primary nociceptive neurons, as well as in substantial slowing-down of this process.