日本名古屋大學研究生院的一個研究小組在英國在線科學期刊《自然—通訊》新一期上報告說，體內(nèi)具有鎮(zhèn)痛作用的內(nèi)源性大麻素會阻礙神經(jīng)軸突獲得再生,。
軸突是動物神經(jīng)元傳導神經(jīng)沖動離開細胞體的細長突起,，是神經(jīng)系統(tǒng)中主要的信號傳遞渠道。如果軸突由于外傷被切斷,，神經(jīng)就無法再發(fā)揮作用,，而且軸突一旦被切斷便很難再生。
名古屋大學研究生院理學研究科副教授久本直毅等研究人員,，將線蟲的軸突切斷后，再將內(nèi)源性大麻素的一種——花生四烯酸乙醇胺注入其體內(nèi),。內(nèi)源性大麻素是體內(nèi)自然產(chǎn)生的類似于大麻的化學物質(zhì),，能“麻醉”神經(jīng)系統(tǒng)。
24小時后,，研究人員將上述線蟲與只切斷了軸突的線蟲進行比較,，發(fā)現(xiàn)注入了花生四烯酸乙醇胺的線蟲軸突沒有再生，而對照組的線蟲軸突則出現(xiàn)再生,。
人體也存在類似的情況,，從以往的研究來看，越是有疼痛感的神經(jīng)越容易恢復,。久本直毅說,，人體內(nèi)也是內(nèi)源性大麻素的量越多，鎮(zhèn)痛效果就越強,，但卻有可能阻礙軸突再生,。如果能抑制這種作用，就有可能開發(fā)出既止痛又不影響神經(jīng)再生的治療方法,。（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.
