Endocannabinoid signaling regulates regenerative axon navigation in C. elegans via the GPCRs NPR-19 and NPR-32.
Endocannabinoid signaling regulates regenerative axon navigation in C. elegans via the GPCRs NPR-19 and NPR-32.
复制标题
内源性大麻素信号通过 GPCR NPR-19 和 NPR-32 调节秀丽隐杆线虫的再生轴突导航。
作者：
Pastuhov;S.;Matsumoto;K.;Hisamoto;N.
神经元的轴突再生能力取决于促进和抑制再生的因素的相互作用。在秀丽隐杆线虫（caenorhabditis elegans）中，JNK MAP激酶（MAPK）通路促进轴突再生。在此之前，我们发现endocannabinoid anandamide （AEA）通过抑制JNK信号通路抑制激光轴突切除后运动神经元的轴突再生反应。在这里，我们发现G蛋白偶联受体（gpcr） NPR - 19和NPR - 32抑制了响应AEA的轴突再生。此外，我们发现感觉神经元表达的编码AEA合成酶的thenape - 1基因，导致再生的运动轴突回避感觉神经元，这种回避反应依赖于NPR - 19和NPR - 32。这些结果表明，AEA对NPR - 19/32 gpcr的作用可调节再生轴突的导航。
The axon regeneration ability of neurons depends on the interplay of factors that promote and inhibit regeneration. InCaenorhabditis elegans, axon regeneration is promoted by the JNK MAP kinase (MAPK) pathway. Previously, we found that the endocannabinoid anandamide (AEA) inhibits the axon regeneration response of motor neurons after laser axotomy by suppressing the JNK signaling pathway. Here, we show that the G‐protein‐coupled receptors (GPCRs) NPR‐19 and NPR‐32 inhibit axon regeneration in response to AEA. Furthermore, we show that sensory neuron expression of thenape‐1gene, which encodes an enzyme synthesizing AEA, causes the regenerating motor axons to avoid sensory neurons and this avoidant response depends on NPR‐19 and NPR‐32. These results indicate that the navigation of regenerating axons is modulated by the action of AEA on NPR‐19/32 GPCRs.