Cross-link of signal transduction and channel function diabetic neuropathy

To Clarify the Mechanism of hyperalgesia in diabetic neuropathy， we investigated the effects of streptozocin-induced hyperglycemia on四氧毒素抵抗Na的D1通道活动的Dorsal root ganglion neurons。实验证明了从链球菌诱导的糖尿病和他们的年龄匹配的控制老鼠中被酶化的神经元的神经元的表现。薄膜电流使用全细胞贴片钳技术进行记录。四毒素耐药性Na的平均当前密度D1+ D-1通道是从糖尿病大鼠控制神经元中准备的信号较大的神经元。Tetrodotoxin-resistant NaイイD1+イエD1 channels were activated at more negative potentials in diabetic than in their control neurons。Curves representing the steady-state inactivation and the peak Na-D1 conductance as function of Oracle brane potential have shifted to the negative side。The changes in gating property of the Na D1 + D1 channel were observed in 6 week after the injection of streptozocin， and still after 8 months糖尿病rats， indicating that tetrodotoxin-resistant Na D1 + D1 channel abnormality starts to developp early and persists during the whole period of diabetes。这些结果表明，神经元参与性神经元在糖尿病动物中的参与是非常有趣的。目前的结果可能会提供一个重要的线索，使糖尿病中的超自然障碍的循环。

To Clarify the mechanism of hyperalgesia in diabetic neuropathy, we investigated the effects of streptozocin-induced hyperglycemia on tetrodotoxin-resistant NaィイD1+ィエD1 channel activity of dorsal root ganglion neurons. Experiments were performed on enzymatically isolated neurons of dorsal root ganglia dissected from streptozocin-induced diabetic and their age-matched control rats. Membrane currents were recorded using the whole-cell patch clamp technique. Mean current density of tetrodotoxin-resistant NaィイD1+ィエD1 channels was significantly larger in neurons prepared from diabetic rats than in their control neurons. Tetrodotoxin-resistant NaィイD1+ィエD1channels were activated at more negative potentials in diabetic than in their control neurons. Curves representing the steady-state inactivation and the peak NaィイD1+ィエD1 conductance as function of membrane potential have shifted to the negative side. The changes in gating property of the NaィイD1+ィエD1 channel were observed in 6 week after the injection of streptozocin, and still after 8 months diabetic rats, indicating that tetrodotoxin-resistant NaィイD1+ィエD1 channel abnormality starts to develop early and persists during the whole period of diabetes. These results suggest that neurons participating in nociception are highly excitable in diabetic animals. The present results may provide an important clue to the elucidation of hyperalgesia in diabetes.