研究人員發(fā)現(xiàn),，大麻使用后的止痛效應(yīng)受藥物中與甘氨酸受體（GlyR）離子通道相連的活性成分四氫大麻酚（THC）所控制,，因此，有望研制出只具有止痛效應(yīng)的四氫大麻酚變體,，新成果發(fā)表在4月在線出版的《自然—化學(xué)生物學(xué)》期刊上,。基于大麻的藥物有興奮和損傷精神活動的副作用,，從而限制了這類藥物未來發(fā)展為止痛藥的可能,；但新研究顯示，修改其中的成分可研制出副作用最小化的新藥,。
大麻即有止痛也有影響精神活性的效應(yīng),，這兩種效應(yīng)均源于它的活性成分四氫大麻酚?？茖W(xué)家們發(fā)現(xiàn),，大麻的精神效應(yīng)受到與大麻受體CB1R聯(lián)接的四氫大麻酚所控制，但他們尚不清楚與止痛效應(yīng)相關(guān)的機制,。Li Zhang和同事發(fā)現(xiàn)了與跨膜區(qū)的GlyR相連接的四氫大麻酚,，以及發(fā)生在四氫大麻酚化學(xué)組分和受體間的氫鍵相互作用。他們還發(fā)現(xiàn),，去除四氫大麻酚的羥基可導(dǎo)致一種不能激活GlyR的化合物,。這些數(shù)據(jù)表明，有可能研制出只激活GlyRs但沒有CB1R活性的四氫大麻酚止痛藥,。（生物谷Bioon.com）
生物谷推薦原文出處：
Nature Chemical Biology doi:10.1038/nchembio.552
Cannabinoid potentiation of glycine receptors contributes to cannabis-induced analgesia
Wei Xiong,1 KeJun Cheng,2 Tanxing Cui,3, 4, 5 Grzegorz Godlewski,6 Kenner C Rice,2 Yan Xu3, 4, 5 & Li Zhang1
Cannabinoids enhance the function of glycine receptors (GlyRs). However, little is known about the mechanisms and behavioral implication of cannabinoid-GlyR interaction. Using mutagenesis and NMR analysis, we have identified a serine at 296 in the GlyR protein critical for the potentiation of IGly by Δ9-tetrahydrocannabinol (THC), a major psychoactive component of marijuana. The polarity of the amino acid residue at 296 and the hydroxyl groups of THC are critical for THC potentiation. Removal of the hydroxyl groups of THC results in a compound that does not affect IGly when applied alone but selectively antagonizes cannabinoid-induced potentiating effect on IGly and analgesic effect in a tail-flick test in mice. The cannabinoid-induced analgesia is absent in mice lacking α3GlyRs but not in those lacking CB1 and CB2 receptors. These findings reveal a new mechanism underlying cannabinoid potentiation of GlyRs, which could contribute to some of the cannabis-induced analgesic and therapeutic effects.
