瘙癢是否疼痛的一種,？數(shù)十年來(lái)未有定論,。美國(guó)約翰斯·霍普金斯大學(xué)研究人員發(fā)現(xiàn)感知瘙癢的神經(jīng)細(xì)胞,，消除了這一疑問(wèn),，有助開(kāi)發(fā)更有效的抗癢藥物和療法,。
鎖定神經(jīng)
約翰斯·霍普金斯大學(xué)神經(jīng)學(xué)家董欣中及其同事借助小鼠實(shí)驗(yàn)尋找感知瘙癢的神經(jīng)細(xì)胞,。研究人員對(duì)小鼠作基因改造，使它們的神經(jīng)細(xì)胞活躍時(shí)變成熒光綠,。他們隨后讓小鼠曝露在刺激性化合物中,，如組胺和癢癢粉的有效成分，鎖定變綠的神經(jīng),。
這些神經(jīng)細(xì)胞遭受過(guò)度刺激時(shí),，小鼠抓撓頻率降低，顯示它們不再覺(jué)得那么癢,。
不過(guò),，這不足以證明那些神經(jīng)只對(duì)瘙癢感作出反應(yīng)。按照先前觀點(diǎn),，那些神經(jīng)也可能對(duì)疼痛感作出反應(yīng),。于是,，研究人員特意刺激小鼠面部感知瘙癢的神經(jīng)細(xì)胞，發(fā)現(xiàn)小鼠用后爪抓撓面部,。這是小鼠感知瘙癢時(shí)的特有反應(yīng),，如果它們覺(jué)得疼痛，就用前肢擦拭面部,。
解決爭(zhēng)論
美國(guó)趣味科學(xué)網(wǎng)站12月27日援引董欣中的話報(bào)道,，實(shí)驗(yàn)結(jié)果顯示，瘙癢神經(jīng)在脊柱內(nèi),，靠近脊髓,，而瘙癢“刺激點(diǎn)”僅存在于皮膚內(nèi)，是人們只想抓撓皮膚而不會(huì)覺(jué)得內(nèi)臟器官瘙癢的原因,，“你不會(huì)覺(jué)得胰腺發(fā)癢”,。
研究結(jié)果由最新一期英國(guó)《自然—神經(jīng)科學(xué)》雜志發(fā)表。
美國(guó)哈佛大學(xué)神經(jīng)學(xué)家伊森·勒納說(shuō),，“這是一項(xiàng)非常令人信服的研究”,，有助于了結(jié)對(duì)瘙癢是否疼痛形式之一的長(zhǎng)期爭(zhēng)論。
董欣中說(shuō),，數(shù)十年來(lái),，瘙癢機(jī)制一直沒(méi)有定論。一些研究發(fā)現(xiàn)某些疼痛神經(jīng)對(duì)瘙癢刺激作出反應(yīng),，而單獨(dú)的瘙癢神經(jīng)難以捕捉,。于是一些人認(rèn)為，瘙癢和疼痛由相同的神經(jīng)纖維感知,，再由大腦作出不同解讀,。但這難以解釋人對(duì)瘙癢和疼痛作出不同反應(yīng)，如遭蚊子叮咬時(shí),，多數(shù)人強(qiáng)烈希望撓一撓,；如果不小心碰到熱爐子，人的直覺(jué)是退縮,。
有助抗癢
勒納說(shuō),，這項(xiàng)研究確認(rèn)了與瘙癢相關(guān)的神經(jīng)纖維，有助研究如何安撫這些神經(jīng),，開(kāi)發(fā)效果更佳的抗癢藥物,。
他說(shuō)，新發(fā)現(xiàn)的意義在于提供抗癢藥物的標(biāo)靶?，F(xiàn)有藥物,，如抗組胺或類固醇，往往通過(guò)消炎發(fā)揮作用,，只能消除小部分瘙癢原因,，如蕁麻疹,。“作為獵槍，類固醇和抗組胺多數(shù)時(shí)候打錯(cuò)目標(biāo),。”
勒納說(shuō)，新發(fā)現(xiàn)的瘙癢神經(jīng)不能解釋所有瘙癢問(wèn)題,，（可能一些神經(jīng)既能感知瘙癢又能感知疼痛,，）但瞄準(zhǔn)那些神經(jīng)可能讓瘙癢治療取得一大進(jìn)步。(生物谷Bioon.com)
doi:10.1038/nn.3289
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A subpopulation of nociceptors specifically linked to itch
Liang Han Chao Ma Qin Liu Hao-Jui Weng Yiyuan Cui Zongxiang Tang Yushin Kim Hong NieLintao Qu Kush N Patel Zhe Li Benjamin McNeil Shaoqiu He Yun Guan Bo Xiao Robert H LaMotte Xinzhong Dong
Itch-specific neurons have been sought for decades. The existence of such neurons has been doubted recently as a result of the observation that itch-mediating neurons also respond to painful stimuli. We genetically labeled and manipulated MrgprA3+ neurons in the dorsal root ganglion (DRG) and found that they exclusively innervated the epidermis of the skin and responded to multiple pruritogens. Ablation of MrgprA3+ neurons led to substantial reductions in scratching evoked by multiple pruritogens and occurring spontaneously under chronic itch conditions, whereas pain sensitivity remained intact. Notably, mice in which TRPV1 was exclusively expressed in MrgprA3+ neurons exhibited itch, but not pain, behavior in response to capsaicin. Although MrgprA3+ neurons were sensitive to noxious heat, activation of TRPV1 in these neurons by noxious heat did not alter pain behavior. These data suggest that MrgprA3 defines a specific subpopulation of DRG neurons mediating itch. Our study opens new avenues for studying itch and developing anti-pruritic therapies.
