Graduate School of Natural Science, Konan University, Kobe, Japan.
Institute for Integrative Neurobiology, Konan University, Kobe, Japan.
EMBO Rep. 2020 Mar 4;21(3):e48671. doi: 10.15252/embr.201948671. Epub 2020 Feb 3.
Caenorhabditis elegans mechanoreceptors located in ASG sensory neurons have been found to sense ambient temperature, which is a key trait for animal survival. Here, we show that experimental loss of xanthine dehydrogenase (XDH-1) function in AIN and AVJ interneurons results in reduced cold tolerance and atypical neuronal response to changes in temperature. These interneurons connect with upstream neurons such as the mechanoreceptor-expressing ASG. Ca imaging revealed that ASG neurons respond to warm temperature via the mechanoreceptor DEG-1, a degenerin/epithelial Na channel (DEG/ENaC), which in turn affects downstream AIN and AVJ circuits. Ectopic expression of DEG-1 in the ASE gustatory neuron results in the acquisition of warm sensitivity, while electrophysiological analysis revealed that DEG-1 and human MDEG1 were involved in warm sensation. Taken together, these results suggest that cold tolerance is regulated by mechanoreceptor-mediated circuit calculation.
秀丽隐杆线虫（Caenorhabditis elegans）中的机械感受器位于 ASG 感觉神经元中，已被发现可以感知环境温度，这是动物生存的关键特征。在这里，我们表明，AIN 和 AVJ 中间神经元中黄嘌呤脱氢酶（XDH-1）功能的实验丧失会导致对寒冷的耐受性降低，以及对温度变化的非典型神经元反应。这些中间神经元与表达机械感受器的 ASG 等上游神经元相连。钙成像显示，ASG 神经元通过机械感受器 DEG-1 对温暖温度做出反应，DEG-1 是一个退行性/上皮钠通道（DEG/ENaC），进而影响下游的 AIN 和 AVJ 回路。ASE 味觉神经元中 DEG-1 的异位表达导致其获得对温暖的敏感性，而电生理分析表明 DEG-1 和人类 MDEG1 参与了温暖感觉。总之，这些结果表明，耐寒性是由机械感受器介导的电路计算调节的。
