發(fā)布時間：2018-04-24 02:22

  本文選題：瘙癢 + 疼痛��； 參考：《中國人民解放軍軍事醫(yī)學(xué)科學(xué)院》2017年博士論文

【摘要】：瘙癢和疼痛是機(jī)體十分重要的兩種感覺,在物種的進(jìn)化過程中比較保守。在生理?xiàng)l件下,短暫的瘙癢和疼痛是一種保護(hù)機(jī)制,它能提示機(jī)體外界的有害刺激,從而做出相應(yīng)的反應(yīng)來避免進(jìn)一步的傷害,比如疼痛主要是引起一種退縮反應(yīng),而瘙癢則引起強(qiáng)烈的抓撓欲望。雖然二者在個人體驗(yàn)以及反應(yīng)形式上差異巨大,但是其并不是完全獨(dú)立的,二者之間存在緊密的聯(lián)系。一些和疼痛相關(guān)的離子通道和受體也介導(dǎo)瘙癢信息的傳遞。隨著瘙癢研究的逐步深入,瘙癢相關(guān)受體和通路逐漸被發(fā)現(xiàn),這些受體參與的瘙癢信息的傳遞也需要部分疼痛相關(guān)離子通道的參與,比如TRPA1和TRPV1。疼痛和瘙癢之間還存在抑制關(guān)系,越來越多的證據(jù)表明疼痛確實(shí)能夠抑制瘙癢,而且一些相關(guān)的抑制通路也陸續(xù)被報道。相比于對疼痛的研究,瘙癢的研究本世紀(jì)以來才有了比較大的進(jìn)展,雖然部分瘙癢相關(guān)的受體、離子通道、神經(jīng)遞質(zhì)以及神經(jīng)元陸續(xù)被發(fā)現(xiàn),但是關(guān)于這些分子的表達(dá)以及相關(guān)神經(jīng)元發(fā)育的調(diào)控機(jī)制,目前來說還很不清楚。一些文獻(xiàn)報道,部分轉(zhuǎn)錄因子參與感覺神經(jīng)元的發(fā)育調(diào)控,我們實(shí)驗(yàn)室前期工作表明轉(zhuǎn)錄因子Tlx3能夠調(diào)控背根神經(jīng)節(jié)中Trk A+神經(jīng)元向Ret+神經(jīng)元的分化,同時也能夠控制一系列疼痛相關(guān)分子的表達(dá)。由于瘙癢感受神經(jīng)元也是來源于Trk A+神經(jīng)元,所以我們猜測Tlx3也能夠調(diào)控瘙癢感受神經(jīng)元的分化發(fā)育以及瘙癢相關(guān)分子的表達(dá)。為了探究這一問題,我們構(gòu)建了Tlx3條件性敲除小鼠Tlx3F/F;Nav1.8-cre,即選擇性地在背根神經(jīng)節(jié)Nav1.8+神經(jīng)元中敲除Tlx3。為了探究轉(zhuǎn)錄因子Tlx3是否會調(diào)控瘙癢相關(guān)分子的表達(dá)水平,我們首先用RNAseq的方法比較了Tlx3條件性敲除小鼠和對照組小鼠背根神經(jīng)節(jié)的轉(zhuǎn)錄組差異,發(fā)現(xiàn)在Tlx3條件性敲除小鼠的背根神經(jīng)節(jié)中大部分目前已經(jīng)報道的瘙癢相關(guān)分子的表達(dá)明顯下降。為了進(jìn)一步驗(yàn)證RNAseq的結(jié)果,我們采用了m RNA原位雜交實(shí)驗(yàn)檢測了部分瘙癢相關(guān)分子的表達(dá),發(fā)現(xiàn)在Tlx3條件性敲除小鼠的背根神經(jīng)節(jié)中Mrgpr A3,IL31ra,Nppb,Sst的表達(dá)完全缺失。以上結(jié)果證明了Tlx3是許多瘙癢相關(guān)分子的表達(dá)所必須的。為了探究Tlx3條件性敲除小鼠背根神經(jīng)節(jié)中瘙癢相關(guān)分子的表達(dá)下調(diào)是否會影響小鼠的瘙癢行為,我們首先比較了Tlx3條件性敲除小鼠和對照組小鼠對多種致癢劑誘導(dǎo)產(chǎn)生的急性瘙癢的反應(yīng)。我們選用了四種不同類型的致癢劑:Compound48/80,chloroquine,α-Me-5-HT,SLIGRL-NH2。Compound48/80能夠引起組胺依賴性瘙癢,而后三種引起非組胺依賴性瘙癢。Tlx3條件性敲除小鼠對這四種致癢劑引起的急性瘙癢的反應(yīng)和對照組小鼠相比都明顯減弱,說明Tlx3能夠調(diào)控急性瘙癢的產(chǎn)生,既包括組胺依賴性瘙癢也包括非組胺依賴性瘙癢。由于許多瘙癢相關(guān)受體也介導(dǎo)慢性瘙癢,所以我們又檢測了Tlx3條件性敲除小鼠對慢性瘙癢的反應(yīng)。我們采用了兩種慢性瘙癢模型:皮膚干燥(Dry skin)和過敏性接觸性皮炎(Allergic contact dermatitis,ACD)模型。Tlx3條件性敲除小鼠對于Dry skin引起的慢性瘙癢的反應(yīng)比對照組小鼠弱,但是對于ACD引起的慢性瘙癢的反應(yīng)卻和對照組小鼠沒有明顯區(qū)別。說明Tlx3也參與調(diào)控部分類型慢性瘙癢的產(chǎn)生。由于許多瘙癢相關(guān)分子的表達(dá)都明顯缺陷,但是Tlx3條件性敲除小鼠仍然出現(xiàn)了明顯的瘙癢,提示慢性瘙癢的復(fù)雜性以及其他信號通路的參與。之前的報道表明在部分慢性瘙癢模型中TRPV1的表達(dá)出現(xiàn)上調(diào),這提示其可能參與慢性瘙癢。我們發(fā)現(xiàn)在Tlx3條件性敲除小鼠和對照組小鼠中TRPV1拮抗劑AMG9810能明顯緩解Dry skin以及ACD引起的慢性瘙癢,表明TRPV1確實(shí)參與慢性瘙癢。疼痛能夠抑制瘙癢,而有報道表明背根神經(jīng)節(jié)中的TRPV1+/TRPA1+神經(jīng)元參與這種抑制,為了探究其是否也受Tlx3調(diào)控,我們使用了辣椒素(capsaicin)和AITC(allyl isothiocyanate)面部注射實(shí)驗(yàn)。我們發(fā)現(xiàn)面部注射AITC在Tlx3條件性敲除小鼠和對照組小鼠都只引起了明顯的疼痛反應(yīng),而幾乎沒有瘙癢反應(yīng),說明抑制通路沒有受到明顯影響。但是面部注射辣椒素在Tlx3條件性敲除小鼠卻引起了明顯增強(qiáng)的疼痛反應(yīng),更意外的是同時也出現(xiàn)了明顯增強(qiáng)的瘙癢�？紤]到抑制通路是正常的,我們認(rèn)為這種明顯增強(qiáng)的瘙癢是由于辣椒素誘導(dǎo)的瘙癢本身增強(qiáng),并且不能完全被抑制通路抑制才表現(xiàn)出來的。由于辣椒素在Tlx3條件性敲除小鼠內(nèi)引起了明顯增強(qiáng)的疼痛和瘙癢,所以我們檢測了辣椒素的受體TRPV1的表達(dá)情況,發(fā)現(xiàn)其表達(dá)量在Tlx3條件性敲除小鼠的背根神經(jīng)節(jié),脊髓以及皮膚中都明顯增加。為了詳細(xì)地了解Tlx3條件性敲除小鼠背根神經(jīng)節(jié)中TRPV1的表達(dá)模式,我們進(jìn)行一系列的免疫熒光實(shí)驗(yàn)。我們發(fā)現(xiàn)在野生型小鼠的背根神經(jīng)節(jié)中只有約27%Tlx3+神經(jīng)元表達(dá)TRPV1而且絕大多數(shù)TRPV1+神經(jīng)元都不表達(dá)或者低表達(dá)Tlx3,進(jìn)一步證實(shí)Tlx3能夠抑制TRPV1的表達(dá)。Tlx3條件性敲除小鼠的背根神經(jīng)節(jié)中TRPV1大幅度地擴(kuò)展到IB4+非肽類神經(jīng)元中,同時其在CGRP+肽類神經(jīng)元的比例也有增加。相似地,在Tlx3條件性敲除小鼠的脊髓背角,TRPV1+神經(jīng)纖維的投射區(qū)域也擴(kuò)展到IB4+神經(jīng)纖維投射區(qū)域即二層內(nèi)側(cè)(lamina IIi)�？紤]到Tlx3能夠調(diào)控許多疼痛相關(guān)受體,而且TRPV1也是感受熱刺激的主要受體之一,所以我們進(jìn)行了一系列疼痛行為學(xué)實(shí)驗(yàn)來探究Tlx3是否調(diào)控疼痛的產(chǎn)生。我們發(fā)現(xiàn)Tlx3條件性敲除小鼠對冷刺激以及炎癥性疼痛的反應(yīng)性明顯下降,而對于機(jī)械,熱刺激以及神經(jīng)病理性疼痛的反應(yīng)卻保持正常。由于TRPV1是目前已知的感受熱的主要受體,雖然其表達(dá)水平在Tlx3條件性敲除小鼠中明顯升高,但是Tlx3條件性敲除小鼠對熱刺激的反應(yīng)卻沒有明顯變化。為了進(jìn)一步驗(yàn)證這一現(xiàn)象,我們采用了脊髓神經(jīng)元激活實(shí)驗(yàn)來判斷熱刺激是否能夠在Tlx3條件性敲除小鼠的脊髓背角激活更多的神經(jīng)元,結(jié)果發(fā)現(xiàn)熱刺激在Tlx3條件性敲除小鼠和對照組小鼠脊髓內(nèi)激活的脊髓神經(jīng)元數(shù)量沒有明顯差別,而辣椒素在Tlx3條件性敲除小鼠脊髓內(nèi)激活的神經(jīng)元數(shù)量卻明顯比對照組小鼠多,說明Tlx3條件性敲除小鼠內(nèi)明顯增加的TRPV1使得其對辣椒素的敏感性增加,卻不影響其對熱刺激的反應(yīng)。綜上,本研究證實(shí)了轉(zhuǎn)錄因子Tlx3能夠調(diào)控大部分瘙癢相關(guān)分子的表達(dá),其功能缺失導(dǎo)致瘙癢相關(guān)分子的表達(dá)下降或者消失,從而使小鼠對急性瘙癢和部分慢性瘙癢的反應(yīng)明顯減弱。Tlx3能夠抑制TRPV1的表達(dá),Tlx3條件性敲除小鼠內(nèi)TRPV1的表達(dá)明顯增加,這就導(dǎo)致面部注射辣椒素在Tlx3條件性敲除小鼠內(nèi)引起了同時增強(qiáng)的疼痛和瘙癢。Tlx3也參與調(diào)控冷痛和炎癥性疼痛的產(chǎn)生。本研究揭示了瘙癢感受神經(jīng)元的發(fā)育的部分分子機(jī)制,同時也證實(shí)了TRPV1在慢性瘙癢產(chǎn)生中的重要性,為以后慢性瘙癢的治療提供了理論依據(jù)。
[Abstract]:Itching and pain are two important senses of the body, which are conservative in the evolutionary process of the species. Under physiological conditions, the transient itching and pain is a protective mechanism that can prompt the harmful stimuli of the body to react to avoid further injury, such as pain mainly causing a retraction reaction, Itching causes strong scratching desire. Although the two are very different in personal experience and form of reaction, but they are not completely independent, there is a close relationship between the two. Some ion channels and receptors associated with pain also mediate the transfer of itching information. With the gradual deepening of itching research, itching related receptors And the pathway has gradually been found that the transfer of these receptors involved in itching information also requires the involvement of partial pain related ion channels, such as the inhibition of TRPA1 and TRPV1. pain and pruritus, and more and more evidence suggests that pain does inhibit itching, and a number of related inhibition pathways are also reported. The study of pain, itching has been a great progress since this century, although some of the pruritus related receptors, ion channels, neurotransmitters and neurons have been discovered, but the expression of these molecules and the regulatory mechanism of the related neuron development are not yet clear. Some reports have reported that some of them have been transferred. Recording factors are involved in the development and regulation of sensory neurons. Our laboratory work indicated that the transcription factor Tlx3 can regulate the differentiation of Trk A+ neurons in the dorsal root ganglia to the Ret+ neurons, and can also control the expression of a series of pain related molecules. As pruritus neurons are derived from Trk A+ neurons, we guessed that Tlx3 can also regulate the differentiation and development of pruritus neurons and the expression of pruritus related molecules. In order to explore this problem, we constructed a Tlx3 conditioned knockout mouse Tlx3F/F; Nav1.8-cre, which selectively knocks off Tlx3. in the Nav1.8+ neurons of the dorsal root ganglia to investigate whether the transcription factor Tlx3 regulates pruritus related points. We first compared the transcriptional groups of the dorsal root ganglion of Tlx3 conditioned knockout mice and control mice by RNAseq method, and found that most of the reported pruritus related molecules in the dorsal root ganglion of Tlx3 conditioned knockout mice were significantly decreased. In order to further verify the results of RNAseq, We used the m RNA in situ hybridization to detect the expression of some pruritus related molecules. We found that the expression of Mrgpr A3, IL31ra, Nppb, Sst in the dorsal root ganglion of Tlx3 conditioned knockout mice was completely missing. The results showed that Tlx3 was necessary for the expression of many pruritus related molecules. In order to explore the dorsal root of Tlx3 conditioned knockout mice Whether the down regulation of pruritus related molecules in the ganglia could affect the itching behavior of mice, we first compared the response of Tlx3 conditioned knockout mice and the control group to the acute itching induced by a variety of itchy agents. We selected four different types of itching agents: Compound48/80, chloroquine, alpha -Me-5-HT, SLIGRL-NH2.Comp Ound48/80 can cause histamine dependent pruritus, and the three types of.Tlx3 conditioned knockout mice that cause unhistamine dependent pruritus decreased the acute pruritus caused by these four itching agents compared with the control group, indicating that Tlx3 can regulate the production of acute itching, including histamine dependent pruritus and non histamine dependent Because many pruritus related receptors also mediate chronic itching, we also detected the response to chronic itching in Tlx3 conditioned knockout mice. We used two chronic pruritus models: Dry skin and allergic contact dermatitis (Allergic contact dermatitis, ACD) model.Tlx3 conditioned knockout mice The response to chronic itching caused by Dry skin was weaker than that in the control group, but the response to chronic itching caused by ACD was not significantly different from that of the control group. It indicated that Tlx3 was also involved in the regulation of some types of chronic pruritus. The expression of many itching related molecules was obviously defective, but the Tlx3 conditional knockout mice were still out. The obvious itching suggests the complexity of chronic itching and the involvement of other signaling pathways. Previous reports suggest that the expression of TRPV1 in some chronic pruritus models is up-regulated, suggesting that it may be involved in chronic itching. We found that the TRPV1 antagonist AMG9810 in Tlx3 conditioned knockout mice and control mice can significantly alleviate D Chronic itching caused by ry skin and ACD indicates that TRPV1 does participate in chronic pruritus. Pain can inhibit itching, and there is a report that TRPV1+/TRPA1+ neurons in the dorsal root ganglion are involved in this inhibition, and to explore whether it is also regulated by Tlx3, we use capsaicin (capsaicin) and AITC (allyl isothiocyanate) facial injection experiments. We found that facial injection of AITC in both Tlx3 conditioned knockout mice and control mice caused only obvious pain responses, and almost no pruritus, indicating that the inhibitory pathway was not significantly affected. However, the facial injection of capsaicin in Tlx3 conditioned knockout mice resulted in significantly enhanced pain responses, and more unexpectedly at the same time. In view of the inhibition pathway is normal, we think this obviously enhanced itching is due to capsaicin induced itching itself, and can not be completely suppressed by inhibition of the pathway. Capsaicin causes significantly enhanced pain and itching in the Tlx3 conditioned knockout rats. So we detected the expression of capsaicin receptor TRPV1 and found that the expression was significantly increased in the dorsal root ganglion, spinal cord and skin of Tlx3 conditioned knockout mice. In order to understand the expression pattern of TRPV1 in the dorsal root ganglion of Tlx3 conditioned knockout mice, we conducted a series of immunofluorescence experiments. Only about 27%Tlx3+ neurons express TRPV1 in the dorsal root ganglion of wild type mice and the overwhelming majority of TRPV1+ neurons do not express or low expression of Tlx3. It is further confirmed that Tlx3 can inhibit TRPV1 expression in the dorsal root ganglion of.Tlx3 conditioned knockout mice, which greatly expand to the IB4+ non peptide neurons, and it is also found in the dorsal root ganglion of.Tlx3 conditioned knockout mice. The proportion of CGRP+ peptide neurons also increased. Similarly, in the dorsal horn of the spinal cord of Tlx3 conditioned knockout mice, the projection area of the TRPV1+ nerve fiber extended to the IB4+ nerve fiber projection area, the two layer (lamina IIi). Considering that Tlx3 can regulate many pain related bodies, TRPV1 is also the main receptor for the sensation of heat stimulation. One of these, so we conducted a series of painful behavioural experiments to explore whether Tlx3 regulates the production of pain. We have found that the response of Tlx3 conditioned knockout mice to cold and inflammatory pain is significantly lower, while the response to mechanical, thermal and neuropathic pain is normal. Because TRPV1 is now known. The main receptor of the sensation of heat, although its expression level was significantly increased in the Tlx3 conditioned knockout mice, but the response of Tlx3 conditioned knockout mice to heat stimulation did not change significantly. In order to further verify this phenomenon, we used the spinal neuron activation experiment to determine whether the heat stimulation could be reduced in Tlx3 conditionality. More neurons were activated in the dorsal horn of the rat's spinal cord. The results showed that the number of neurons activated in the spinal cord of the Tlx3 conditioned knockout mice and the control group was not significantly different, but the number of neurons activated in the spinal cord of Tlx3 conditioned knockout mice was significantly more than that of the control group, indicating that the Tlx3 conditionality was knocked out. The increased sensitivity of TRPV1 to capsaicin in mice increased its sensitivity to capsaicin, but did not affect its response to thermal stimulation. In this study, this study confirmed that the transcription factor Tlx3 can regulate the expression of most pruritus related molecules, whose function loss causes the expression of pruritus related molecules to descend or disappear, thus causing acute itching and part of the mice to the Ministry. The response to chronic pruritus significantly weakened the expression of.Tlx3, which inhibited the expression of TRPV1, and the expression of TRPV1 in Tlx3 conditioned knockout mice increased significantly, which resulted in the increased pain and itching of the capsaicin in Tlx3 conditioned knockout mice, which also involved the regulation of cold pain and inflammatory pain. The molecular mechanism of the development of pruritus sensory neurons also confirms the importance of TRPV1 in the production of chronic itching and provides a theoretical basis for the treatment of chronic itching.

【學(xué)位授予單位】：中國人民解放軍軍事醫(yī)學(xué)科學(xué)院
【學(xué)位級別】：博士
【學(xué)位授予年份】：2017
【分類號】：R338

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