LAUSR

To study whether diabetes mellitus (DM) would cause electrophysiological alterations in nodose ganglion (NG) neurons, we used patch clamp and intracellular recording for voltage and current clamp configuration, respectively, on cell bodies of NG from rats with DM. Intracellular microelectrodes recording, according to the waveform of the first derivative of the action potential, revealed three neuronal groups (A0, Ainf, and Cinf), which were differently affected. Diabetes only depolarized the resting potential of A0 (from −55 to −44 mV) and Cinf (from −49 to −45 mV) somas. In Ainf neurons, diabetes increased action potential and the after‐hyperpolarization durations (from 1.9 and 18 to 2.3 and 32 ms, respectively) and reduced dV/dtdesc (from −63 to ‐52 V s−1). Diabetes reduced the action potential amplitude while increasing the after‐hyperpolarization amplitude of Cinf neurons (from 83 and −14 mV to 75 and −16 mV, respectively). Using whole cell patch clamp recording, we observed that diabetes produced an increase in peak amplitude of sodium current density (from −68 to −176 pA pF−1) and displacement of steady‐state inactivation to more negative values of transmembrane potential only in a group of neurons from diabetic animals (DB2). In the other group (DB1), diabetes did not change this parameter (−58 pA pF−1). This change in sodium current did not cause an increase in membrane excitability, probably explainable by the alterations in sodium current kinetics, which are also induced by diabetes. Our data demonstrate that diabetes differently affects membrane properties of different nodose neuron subpopulations, which likely have pathophysiological implications for diabetes mellitus.