日本名古屋大学研究生院的一个研究小组在英国在线科学期刊《自然—通讯》新一期上报告说，体内具有镇痛作用的内源性大麻素会阻碍神经轴突获得再生。
轴突是动物神经元传导神经冲动离开细胞体的细长突起，是神经系统中主要的信号传递渠道。如果轴突由于外伤被切断，神经就无法再发挥作用，而且轴突一旦被切断便很难再生。
名古屋大学研究生院理学研究科副教授久本直毅等研究人员，将线虫的轴突切断后，再将内源性大麻素的一种——花生四烯酸乙醇胺注入其体内。内源性大麻素是体内自然产生的类似于大麻的化学物质，能“麻醉”神经系统。
24小时后，研究人员将上述线虫与只切断了轴突的线虫进行比较，发现注入了花生四烯酸乙醇胺的线虫轴突没有再生，而对照组的线虫轴突则出现再生。
人体也存在类似的情况，从以往的研究来看，越是有疼痛感的神经越容易恢复。久本直毅说，人体内也是内源性大麻素的量越多，镇痛效果就越强，但却有可能阻碍轴突再生。如果能抑制这种作用，就有可能开发出既止痛又不影响神经再生的治疗方法。（生物谷Bioon.com）
doi: 10.1038/ncomms2136
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Endocannabinoid-Goα signalling inhibits axon regeneration in Caenorhabditis elegans by antagonizing Gqα-PKC-JNK signalling.
Pastuhov SI, Fujiki K, Nix P, Kanao S, Bastiani M, Matsumoto K, Hisamoto N.
The ability of neurons to regenerate their axons after injury is determined by a balance between cellular pathways that promote and those that inhibit regeneration. In Caenorhabditis elegans, axon regeneration is positively regulated by the c-Jun N-terminal kinase mitogen activated protein kinase pathway, which is activated by growth factor-receptor tyrosine kinase signalling. Here we show that fatty acid amide hydrolase-1, an enzyme involved in the degradation of the endocannabinoid anandamide (arachidonoyl ethanolamide), regulates the axon regeneration response of γ-aminobutyric acid neurons after laser axotomy. Exogenous arachidonoyl ethanolamide inhibits axon regeneration via the Goα subunit GOA-1, which antagonizes the Gqα subunit EGL-30. We further demonstrate that protein kinase C functions downstream of Gqα and activates the MLK-1-MEK-1-KGB-1 c-Jun N-terminal kinase pathway by phosphorylating MLK-1. Our results show that arachidonoyl ethanolamide induction of a G protein signal transduction pathway has a role in the inhibition of post-development axon regeneration.
