UNIVERSITY OF BUCHAREST
FACULTY OF PHYSICS

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Conference: Bucharest University Faculty of Physics 2009 Meeting


Section: Biophysics; Medical Physics


Title:
TTX-sensitive and TTX-resistant sodium channels in type I diabetes


Authors:
Beatrice Mihaela Radu (1), Mihai Radu (2)


Affiliation:
(1)Department of Animal Physiology and Biophysics, Center of Neurobiology and Molecular Physiology, Faculty of Biology, University of Bucharest, Splaiul Independentei, 91-95, Bucharest, 050095, Romania

(2) Department of Health and Environmental Physics, ‘Horia Hulubei’ National Institute for Physics and Nuclear Engineering, Atomistilor, 407, Măgurele, 077125, Romania


E-mail
beatrice_macri@yahoo.com


Keywords:
sensory neurons, TTX-R, TTX-S, genetic diabetes


Abstract:
Voltage-gated sodium channels are heteromultimers of a large pore-forming α-subunit and smaller auxiliary β-subunits. Nine distinct genes (SCN1A–5A, SCN8A–11A) encode the Nav1.1–Nav1.9 channels. Sodium channels are responsible for the generation and propagation of action potentials in excitable cells in response to membrane depolarization. Sodium channels can be distinguished by the voltage-dependence and kinetics of their transition between these states, and pharmacologically according to their sensitivity to the toxin tetrodotoxin (TTX. Most of the neuronal channels are sensitive to nanomolar concentrations of TTX (TTX-S, while the cardiac channel Nav1.5 and the sensory neuron-specific channels Nav1.8 and Nav1.9 are resistant to 100–1000 fold higher concentrations of TTX (TTX-R. In our study, we have used sensory neurons from dorsal root ganglia prelevated from TRC-HA+/-/Ins-HA+/- mice and Balb/c. Immunofluorescence assays on Nav 1.5, Nav 1.7, Nav 1.8 receptors have been performed. The level of expression for Nav 1.5 and Nav 1.8 is decreased by diabetes, while the level of Nav 1.7 is increased. By means of electrophysiological recordings (patch-clamp technique), we have demonstrated that the ionic currents through these sodium channels are also modified in diabetic conditions. This study was financed by PNCDI2 41-074/2007.