BEATRICE MIHAELA RADU*, ADINA DANIELA IANCU*,**, ADELA MARIN*, M. RADU***, D.D. BANCIU*, CRINA STAVARU**, D.L. RADU**
*Department of Animal Physiology and Biophysics, Center of Neurobiology and Molecular Physiology, Faculty of Biology, University of Bucharest, 91–95, Splaiul Independenţei, Bucharest, 050095, Romania, email@example.com
**Laboratory of Cellular Immunity, “Cantacuzino” National Institute for Microbiology and Immunology, 103, Splaiul Independenţei, Bucharest, 050096, Romania
***Department of Health and Environmental Physics, “Horia Hulubei” National Institute for Physics and Nuclear Engineering, PO Box MG6, Măgurele, 077125, Romania
Abstract. Despite the increased prevalence of peripheral diabetic neuropathy, some of its mechanisms are still unknown. In our study, we have used a double transgenic mice (dTg) model, TCR-HA+/–/RIP-HA+/–, which develops a fulminate type of insulino-dependent diabetes. The goal of our study was to reveal the molecular mechanisms of diabetic neuropathy in neuronal primary cultures. The presence of the transgenes, that are responsible for the etiophatogenesis of type I diabetes is determined by the PCR technique. Blood glucose, insulin level and corporal weight are monitored after 4 weeks of life. Neuronal primary cultures are dissociated from dorsal root ganglia. Electrophysiological recordings of these neurons are performed by patch-clamp technique, whole-cell configuration. In our study we have recorded the characteristics of the action potential and the hyperpolarization activated currents in sensory neurons. Significant differences were evidenced between the electrophysiological profiles of the sensory neurons from dorsal root ganglia prelevated from TCR-HA+/– / RIP-HA+/– mice compared to BALB/c mice.
Key words: type I diabetes, sensory neurons, action potential, Ih current.
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