Painful diabetic neuropathy (PDN), a chronic and often incurable syndrome, is one of the most common and unpleasant complications of diabetes. Effective clinical interventions for PDN are very limited and already developed approaches are characterized by lack of molecular or cellular target specificity and a short duration of therapeutic effects. Numerous investigations causally link upregulation of Cav3.2 T-type Ca2+ channels in peripheral nociceptive neurons to painful symptoms of PDN. Here we suggest an approach, based on implementation of virus-mediated cell-specific delivery of vectors expressing small hairpin RNAs (shRNAs). Processed by Dicer into specific small interfering RNA (siRNA), they would suppress the translation of T-type Ca2+ channels, in this way alleviating PDN symptoms. In order to experimentally validate this approach we have chosen several programmatically-designed Dicer-substrate small interfering RNAs (DsiRNAs), which should be effective in suppression of the Cav3.2 expression. Primary cultures of rat hippocampus were established and transfected with DsiRNAs. Ca2+-imaging coupled with neuron stimulation in the current-clamp mode was used to estimate the decrease in the expression of the Cav3.2 channels based on the values of the T-type channel-mediated transients of intracellular Ca2+ concentration. We have shown that one of the developed DsiRNAs suppressed T-type channel-mediated transients indicating possible interference of that DsiRNA variant with the Cav3.2 mRNA translation. This DsiRNA will be further used for both direct spinal nerve injections and designing shRNA-coding sequence for the cloning into AAV6 vector-based expression construct for the cell-specific delivery to nociceptive neurons. Supported by NRFU grant # 2021.01/0435.