Laboratory of Electrophysiology, Superior Institute of Biomedical Sciences, State University of Ceará, Fortaleza, Brazil.
Technological and Exact Science Center, State University Vale do Acaraú, Sobral, Brazil.
Physiol Rep. 2023 Feb;11(4):e15605. doi: 10.14814/phy2.15605.
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 (A , A , and C ), which were differently affected. Diabetes only depolarized the resting potential of A (from -55 to -44 mV) and C (from -49 to -45 mV) somas. In A 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/dt (from -63 to -52 V s ). Diabetes reduced the action potential amplitude while increasing the after-hyperpolarization amplitude of C 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 ) 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 ). 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.
为了研究糖尿病（DM）是否会导致迷走神经节（NG）神经元的电生理改变，我们使用膜片钳技术，分别对 DM 大鼠的 NG 细胞体进行电压和电流钳位记录。根据动作电位一阶导数的波形，细胞内微电极记录显示出三个不同的神经元群体（A 、A 和 C ），它们受到不同的影响。糖尿病仅使 A （从-55 至-44mV ）和 C （从-49 至-45mV ）神经元的静息电位去极化。在 A 神经元中，糖尿病增加了动作电位和超极化后电位的持续时间（分别从 1.9 和 18 至 2.3 和 32ms ），并降低了 dv/dt （从-63 至-52V s ）。糖尿病降低了 A 神经元的动作电位幅度，同时增加了 C 神经元的超极化后电位幅度（分别从 83 和-14mV 至 75 和-16mV ）。使用全细胞膜片钳记录，我们观察到糖尿病增加了钠电流密度的峰值幅度（从-68 至-176pA pF ），并将稳态失活向跨膜电位的更负值转移，这仅发生在一组来自糖尿病动物的神经元中（DB2 ）。在另一组（DB1 ）中，糖尿病没有改变这个参数（-58pA pF ）。这种钠电流的变化并没有引起膜兴奋性的增加，这可能是由于钠电流动力学的改变，而这种改变也是由糖尿病引起的。我们的数据表明，糖尿病对不同迷走神经节神经元亚群的膜特性有不同的影响，这可能对糖尿病有病理生理学意义。
