AP-2蛋白在小鼠耳蝸毛細(xì)胞的表達(dá)及其調(diào)控突觸囊泡胞吞的實(shí)驗(yàn)研究
發(fā)布時(shí)間：2018-07-18 15:57
【摘要】：一、研究背景和目的感音神經(jīng)性耳聾是最常見(jiàn)的聽(tīng)覺(jué)殘疾,聽(tīng)覺(jué)的產(chǎn)生和維持依賴于耳蝸內(nèi)毛細(xì)胞(IHC)帶狀突觸部釋放谷氨酸神經(jīng)遞質(zhì),由此完成機(jī)械-電換能作用[1]。作為聽(tīng)覺(jué)傳導(dǎo)第一級(jí)突觸,耳蝸IHC突觸發(fā)生病理改變是導(dǎo)致感音神經(jīng)性耳聾的重要原因之一[2,3]。大量研究表明,聽(tīng)功能的減退與帶狀突觸形態(tài)、結(jié)構(gòu)和數(shù)量的異常變化密切相關(guān)[3]。每個(gè)IHC與螺旋神經(jīng)元建立一個(gè)突觸連接,單個(gè)IHC擁有10-30個(gè)帶狀突觸。耳蝸IHC帶狀突觸活性區(qū)域的快速可釋放池(RRP)釋放出的神經(jīng)遞質(zhì)谷氨酸激活位于突觸后膜的谷氨酸受體(AMPA),將聽(tīng)覺(jué)信息傳遞給蝸核的對(duì)應(yīng)神經(jīng)元[4]�？梢�(jiàn),耳蝸感受到的絕大部分聲信號(hào)是靠IHC及其突觸完成的。每個(gè)RRP有數(shù)十個(gè)囊泡附著,可在幾微秒內(nèi)釋放囊泡,大量囊泡的同步釋放可通過(guò)興奮性突觸后電位(EPSPs)反映[5]。根據(jù)聽(tīng)覺(jué)信號(hào)傳導(dǎo)的特點(diǎn),IHC突觸精確快速地傳遞神經(jīng)遞質(zhì)需要正常有效的囊泡循環(huán)機(jī)制,即囊泡的胞吐和胞吞[6]。突觸囊泡循環(huán)(recycling)是聽(tīng)覺(jué)神經(jīng)遞質(zhì)持續(xù)釋放的基礎(chǔ),而突觸囊泡精確快速的內(nèi)吞回收則是囊泡信息持續(xù)傳遞不被耗竭的重要保障。網(wǎng)格蛋白介導(dǎo)的內(nèi)吞(CME)途徑是中樞神經(jīng)細(xì)胞突觸囊泡膜回收的重要方式[7],AP-2蛋白為內(nèi)吞起始階段識(shí)別網(wǎng)格蛋白和協(xié)同其它輔助蛋白形成網(wǎng)格蛋白包被小泡(coated pits)的結(jié)構(gòu)核心,它是由α、β2、μ2和σ2四個(gè)亞基組成的大的蛋白復(fù)合體,α亞基附件區(qū)域與質(zhì)膜形成聯(lián)系,同時(shí)通過(guò)DPF或者DPW分子信號(hào)與多種調(diào)控蛋白和輔助蛋白結(jié)合;β2亞基與網(wǎng)格蛋白β螺旋末端結(jié)構(gòu)域結(jié)合,還與轉(zhuǎn)運(yùn)貨物(cargo)的選擇相關(guān);μ2亞基通過(guò)酪氨酸分類信號(hào)識(shí)別胞質(zhì)尾區(qū)受體[8]。AP-2蛋白在CME內(nèi)吞起始階段發(fā)揮著重要作用。耳蝸IHC及其傳入神經(jīng)元作為一種特殊的神經(jīng)突觸,AP-2蛋白調(diào)控CME途徑理論上應(yīng)該在此區(qū)域發(fā)揮著重要作用。目前關(guān)于AP-2蛋白的研究多局限于它的蛋白組學(xué)和它在中樞神經(jīng)細(xì)胞的研究,AP-2蛋白在小鼠耳蝸中的定位表達(dá)及功能關(guān)系尚不清楚。本研究擬應(yīng)用免疫熒光雙重標(biāo)記,激光共聚焦顯微鏡觀察ap-2蛋白與帶狀突觸前膜特異性蛋白rebeye/ctbp2在小鼠耳蝸毛細(xì)胞中的定位表達(dá)特點(diǎn),探討其在內(nèi)耳聽(tīng)覺(jué)生理中的可能作用機(jī)制。再結(jié)合聽(tīng)性腦干反應(yīng)(abr),熒光定量pcr(qrt-pcr)觀察出生后不同發(fā)育階段ap-2蛋白的表達(dá),探討ap-2蛋白與聽(tīng)功能的發(fā)生、形成和年齡相關(guān)性聽(tīng)力減退的相關(guān)性。最后通過(guò)膜片鉗電生理方法,采用tyrphostina23(酪氨酸磷酸化抑制劑a23)抑制ap-2蛋白的銜接功能,進(jìn)而影響cme的胞吞作用,通過(guò)研究ap-2蛋白的特異性抑制致小鼠耳蝸ihc電生理的改變情況,初步探討ap-2蛋白在耳蝸ihc突觸囊泡胞吞的可能作用機(jī)制,為研究感音神經(jīng)性耳聾在蛋白質(zhì)水平的發(fā)病機(jī)制提供參考。二、材料與方法1、選擇健康成年c57bl/6j(8周齡)小鼠20只,耳廓反應(yīng)靈敏,abr閾值正常。通過(guò)ap-2和dapi雙重標(biāo)記以及ap-2、ctbp2和dapi三重標(biāo)記,應(yīng)用免疫熒光標(biāo)記技術(shù)結(jié)合激光共聚焦顯微鏡觀察ap-2蛋白在耳蝸毛細(xì)胞的定位與表達(dá)。2、選用7、15、35日、及16月齡小鼠各20只,分別代表新生小鼠、聽(tīng)功能發(fā)育階段小鼠、聽(tīng)功能發(fā)育成熟小鼠及老年性小鼠,通過(guò)免疫熒光激光共聚焦顯微鏡,qrt-pcr技術(shù)檢測(cè)基底膜內(nèi)毛細(xì)胞ap-2蛋白的表達(dá)特點(diǎn),結(jié)合abr測(cè)定小鼠聽(tīng)閾等討論聽(tīng)功能的發(fā)生、形成、以及年齡相關(guān)性聽(tīng)功能減退與小鼠耳蝸ap-2蛋白表達(dá)的相關(guān)性。3、通過(guò)tyrphostina23(酪氨酸磷酸化抑制劑a23)抑制yxxФ分子信號(hào)與ap-2μ2亞基的相互作用,分析內(nèi)毛細(xì)胞ap-2蛋白被特異性抑制后小鼠ihc電生理的改變情況,從而反映ap-2蛋白對(duì)cme的影響。三、結(jié)果:1、ap-2蛋白屬于細(xì)胞胞漿蛋白,主要表達(dá)于ihc突觸活化部位,濃集于胞質(zhì)基底外側(cè),靠近傳入神經(jīng)元區(qū)域。ap-2蛋白表達(dá)的形態(tài)學(xué)定位位點(diǎn)與其調(diào)控cme途徑的功能學(xué)相映襯。2、abr閾值測(cè)定發(fā)現(xiàn),p15、p35、16月齡小鼠聽(tīng)閾分別為18.67±1.21dbnhl,13.83±1.47dbnhl和37.83±7.68dbnhl,p7組小鼠聽(tīng)力尚未引出。軟件計(jì)算p7、p15、p35及16月齡組熒光染色密度值(imv)分別為:190.91±17.27,494.06±27.63,838.41±38.23,682.65±72.22;qrt-pcr測(cè)定p7、p15、p35及16月齡組ap-2mrna相對(duì)表達(dá)量(rq)分別為0.53±0.09,1.03±0.02,1.00±0.09,1.03±0.06。p7與p15組比較,隨著聽(tīng)功能的產(chǎn)生和形成,免疫熒光光密度值和ap-2mrna相對(duì)表達(dá)量均提示AP-2的表達(dá)水平明顯升高,差異具有統(tǒng)計(jì)學(xué)意義(P0.05);P35與16月齡組比較,老年組AP-2蛋白熒光光密度值減少,然而通過(guò)q RT-PCR分析兩者AP-2 mRNA的表達(dá)水平,差異無(wú)明顯統(tǒng)計(jì)學(xué)意義(P0.05)。3、通過(guò)Tyrphostin A23的抑制作用,AP-2蛋白的銜接功能受阻礙,進(jìn)而影響CME路徑,IHC電壓依賴性Ca2+通道開(kāi)放和關(guān)閉延遲,ICa2+減小,△Cm降低,IHC膜電容及鈣電流的改變表明AP-2蛋白調(diào)控的CME途徑在IHC突觸區(qū)域參與了囊泡的內(nèi)吞作用。四、結(jié)論1、AP-2蛋白在成年小鼠耳蝸中主要表達(dá)于IHC突觸活化區(qū)域,形態(tài)學(xué)的定位位點(diǎn)與其調(diào)控CME途徑的功能學(xué)相符合,間接反映了AP-2蛋白與突觸的關(guān)聯(lián)及意義,它可能在IHC突觸囊泡的內(nèi)吞中發(fā)揮著重要作用,為深入探索AP-2蛋白在內(nèi)耳聽(tīng)覺(jué)生理和病理中的作用奠定了基礎(chǔ)。2、AP-2蛋白在小鼠內(nèi)耳發(fā)育不同階段均有不等強(qiáng)度的表達(dá),新生小鼠至聽(tīng)力的產(chǎn)生和發(fā)育成熟階段,耳蝸AP-2蛋白隨小鼠日齡增大而表達(dá)增強(qiáng),提示AP-2蛋白的表達(dá)水平可能與聽(tīng)功能的發(fā)生、形成和維持密切相關(guān)。3、特異性抑制AP-2蛋白的功能,能影響CME途徑,突觸間隙內(nèi)神經(jīng)遞質(zhì)不能被IHC突觸前膜有效地內(nèi)吞回收,影響了突觸循環(huán),最終影響了IHC神經(jīng)遞質(zhì)的釋放。說(shuō)明AP-2蛋白在調(diào)控小鼠耳蝸IHC的突觸囊泡回收中發(fā)揮著重要重要。
[Abstract]:First, research background and purpose sensorineural deafness is the most common auditory disability. The generation and maintenance of hearing depends on the release of glutamate neurotransmitters in the IHC band synapses, thus completing the mechanical and electrical energy transfer function [1]. as the first stage of auditory conduction, and the pathological changes in the cochlear IHC synapse cause the sensorineural nerve. One of the important causes of sexual deafness [2,3]. a large number of studies have shown that the hypofunction of auditory function is closely related to the abnormal changes in the form of banded synapses, structure and number of [3]., each IHC has a synaptic connection with the spiral neurons, and a single IHC has 10-30 banded synapses. The rapid release pool (RRP) of the cochlear IHC stripline contact area is released from the cochlea (RRP). The neurotransmitter glutamic acid activates the glutamate receptor (AMPA) in the postsynaptic membrane, which passes the auditory information to the corresponding neuron [4]. in the cochlear nucleus. Most of the acoustic signals are accomplished by IHC and its synapses. Ten vesicles per RRP are attached to each RRP, and the vesicles can be released in a few microseconds and the simultaneous release of a large number of vesicles can be obtained. Through the excitatory postsynaptic potential (EPSPs) reflecting the characteristics of [5]. based on auditory signal transduction, the precise and rapid transmission of neurotransmitters in IHC synapses requires a normal and effective vesicle cycle mechanism, namely, vesicular exocytosis and endocytosis of [6]. synaptic vesicle cycle (recycling), which is the basis for the continuous release of auditory nerve transmitters, and synaptic vesicles are accurate and fast within. The endocytosis recovery is an important guarantee for the continuous transmission of vesicle information. The CME pathway is an important way for the recovery of synaptic vesicles in central nervous cells, [7], and AP-2 protein is the structural core of the identification of gridin in the endocytic initial stage and the formation of a lrellin envelope (coated pits) with other auxiliary proteins. The heart, which is a large protein complex consisting of four subunits of alpha, beta 2, 2, and sigma 2, is associated with the plasma membrane of the appendage region of the alpha subunit, and is combined with a variety of regulatory proteins and auxiliary proteins by DPF or DPW molecular signals; the beta 2 subunit is associated with the helix terminal domain of the gridin beta, and is related to the selection of the transport goods (cargo); and the subunit of the mu 2 subunit. The identification of the cytoplasmic tail region receptor [8].AP-2 protein by the tyrosine classification signal plays an important role in the initial stage of the endocytic endocytosis. The cochlear IHC and its afferent neurons act as a special synapse, and the AP-2 protein regulation of the CME pathway should play an important role in this region. The study of the AP-2 protein before the eye is mostly limited to it. In the study of proteomics and its central nervous cells, the expression and function of AP-2 protein in the mouse cochlea are not clear. This study intends to use double immunofluorescence labeling and laser confocal microscopy to observe the localization and expression characteristics of AP-2 protein and the banded presynaptic specific protein rebeye/ctbp2 in the mouse cochlear hair cells To explore the possible mechanism of its possible action in the auditory physiology of the inner ear, the expression of AP-2 protein in different developmental stages after birth was observed with auditory brainstem response (ABR) and fluorescence quantitative PCR (qRT-PCR). The correlation between the occurrence of AP-2 protein and hearing function and the correlation of age related hearing loss was discussed. Finally, the electrophysiological method of patch clamp was used to use Tyr. Phostina23 (tyrosine phosphorylation inhibitor A23) inhibits the cohesive function of AP-2 protein and affects the endocytosis of CME. The possible mechanism of AP-2 protein in the cochlear IHC synaptic vesicle swallowing is preliminarily discussed by studying the specific inhibition of the IHC electrophysiology of the mouse cochlea by the specific inhibition of the AP-2 protein, so as to study the sensorineural deafness in the egg. Two, materials and methods 1, materials and methods 1, select 20 healthy adult c57bl/6j (8 weeks old) mice, the auricle is sensitive and the ABR threshold is normal. By AP-2 and DAPI double markers and AP-2, ctbp2 and DAPI three markers, the immunofluorescent labeling technique combined with laser confocal microscope to observe the cochlear capillary of AP-2 protein The location and expression of.2, 7,15,35 day, and 20 mice in 16 month old mice, respectively representing newborn mice, hearing functional development mice, hearing functional mature mice and senile mice, using immunofluorescent laser confocal microscopy, qRT-PCR technique to detect the expression of AP-2 protein in the basal membrane of the hair cells, and ABR for the determination of the mouse hearing. Threshold, etc., to discuss the occurrence, formation of auditory function, and the correlation of age related impairment of auditory function with the expression of AP-2 protein in the cochlea of mice, and the inhibition of the interaction between the yxx molecular signal and AP-2 2 subunit by tyrphostina23 (tyrosine phosphorylation inhibitor A23), and the analysis of the electrophysiological changes of IHC in the mouse after the specific inhibition of the internal capillary cell AP-2 protein. Change the situation to reflect the effect of AP-2 protein on CME. Three, results: 1, AP-2 protein belongs to cytoplasmic protein, mainly expressed in the activation site of IHC synapse, which is concentrated in the lateral of cytoplasm basement. The morphological loci of the.Ap-2 protein expression near the afferent neuron region reflect the function of CME pathway, and the ABR threshold determination is found, p15 The hearing threshold of p35,16 months of age in mice was 18.67 + 1.21dbnhl, 13.83 + 1.47dbnhl and 37.83 + 7.68dbnhl, and the hearing loss in P7 group was not elicited. The software P7, p15, p35 and 16 month old groups of fluorescent staining density values (IMV) were 190.91 + 17.27494.06 + 27.63838.41 + 38.23682.65 72.22, respectively. The amount of RQ was 0.53 + 0.09,1.03 + 0.02,1.00 + 0.09,1.03 + 0.06.p7 and p15 group respectively. With the emergence and formation of auditory function, the expression of immunofluorescence light density and ap-2mrna relative expression suggested that the expression level of AP-2 increased significantly, and the difference was statistically significant (P0.05); P35 and the 16 month old groups were compared with the fluorescent light density of the AP-2 protein in the elderly group. However, the expression level of AP-2 mRNA was analyzed by Q RT-PCR, and the difference was not statistically significant (P0.05).3. The cohesive function of AP-2 protein was hindered by the inhibition of Tyrphostin A23, and then the CME path was hindered, the IHC voltage dependent Ca2+ channel opening and closing delay, the decrease of delta, the capacitance and the calcium current were reduced. The changes indicated that the CME pathway regulated by AP-2 protein participates in the endocytosis of vesicles in the IHC synaptic region. Four, conclusion 1, AP-2 protein is mainly expressed in the IHC synaptic activation region in adult mouse cochlea. The location of the morphologic loci is in accordance with the function of the CME pathway, which reflects the Association and significance of the AP-2 protein with the synapse. It may play an important role in the endocytosis of IHC synaptic vesicles, which lays a foundation for the in-depth exploration of the role of AP-2 protein in the auditory physiology and pathology of the inner ear. The AP-2 protein has unequal intensity expression in different stages of the development of the inner ear of mice, the generation of newborn mice to hearing and the mature stage, and the AP-2 protein of the cochlea with the age of mice. The expression of AP-2 protein may be enhanced, suggesting that the expression level of the protein may be related to the occurrence of auditory function, the formation and maintenance of the closely related.3, the specific inhibition of the function of the AP-2 protein and the influence of the CME pathway. The neurotransmitters in the synaptic gap can not be effectively recovered from the IHC presynaptic membrane, which affects the synaptic cycle and ultimately affects the release of the IHC neurotransmitter. It indicates that AP-2 protein plays an important role in regulating the recovery of synaptic vesicles in mouse cochlea IHC.
【學(xué)位授予單位】：第三軍醫(yī)大學(xué)
【學(xué)位級(jí)別】：碩士
【學(xué)位授予年份】：2015
【分類號(hào)】：R764.35
本文編號(hào)：2132404
[Abstract]:First, research background and purpose sensorineural deafness is the most common auditory disability. The generation and maintenance of hearing depends on the release of glutamate neurotransmitters in the IHC band synapses, thus completing the mechanical and electrical energy transfer function [1]. as the first stage of auditory conduction, and the pathological changes in the cochlear IHC synapse cause the sensorineural nerve. One of the important causes of sexual deafness [2,3]. a large number of studies have shown that the hypofunction of auditory function is closely related to the abnormal changes in the form of banded synapses, structure and number of [3]., each IHC has a synaptic connection with the spiral neurons, and a single IHC has 10-30 banded synapses. The rapid release pool (RRP) of the cochlear IHC stripline contact area is released from the cochlea (RRP). The neurotransmitter glutamic acid activates the glutamate receptor (AMPA) in the postsynaptic membrane, which passes the auditory information to the corresponding neuron [4]. in the cochlear nucleus. Most of the acoustic signals are accomplished by IHC and its synapses. Ten vesicles per RRP are attached to each RRP, and the vesicles can be released in a few microseconds and the simultaneous release of a large number of vesicles can be obtained. Through the excitatory postsynaptic potential (EPSPs) reflecting the characteristics of [5]. based on auditory signal transduction, the precise and rapid transmission of neurotransmitters in IHC synapses requires a normal and effective vesicle cycle mechanism, namely, vesicular exocytosis and endocytosis of [6]. synaptic vesicle cycle (recycling), which is the basis for the continuous release of auditory nerve transmitters, and synaptic vesicles are accurate and fast within. The endocytosis recovery is an important guarantee for the continuous transmission of vesicle information. The CME pathway is an important way for the recovery of synaptic vesicles in central nervous cells, [7], and AP-2 protein is the structural core of the identification of gridin in the endocytic initial stage and the formation of a lrellin envelope (coated pits) with other auxiliary proteins. The heart, which is a large protein complex consisting of four subunits of alpha, beta 2, 2, and sigma 2, is associated with the plasma membrane of the appendage region of the alpha subunit, and is combined with a variety of regulatory proteins and auxiliary proteins by DPF or DPW molecular signals; the beta 2 subunit is associated with the helix terminal domain of the gridin beta, and is related to the selection of the transport goods (cargo); and the subunit of the mu 2 subunit. The identification of the cytoplasmic tail region receptor [8].AP-2 protein by the tyrosine classification signal plays an important role in the initial stage of the endocytic endocytosis. The cochlear IHC and its afferent neurons act as a special synapse, and the AP-2 protein regulation of the CME pathway should play an important role in this region. The study of the AP-2 protein before the eye is mostly limited to it. In the study of proteomics and its central nervous cells, the expression and function of AP-2 protein in the mouse cochlea are not clear. This study intends to use double immunofluorescence labeling and laser confocal microscopy to observe the localization and expression characteristics of AP-2 protein and the banded presynaptic specific protein rebeye/ctbp2 in the mouse cochlear hair cells To explore the possible mechanism of its possible action in the auditory physiology of the inner ear, the expression of AP-2 protein in different developmental stages after birth was observed with auditory brainstem response (ABR) and fluorescence quantitative PCR (qRT-PCR). The correlation between the occurrence of AP-2 protein and hearing function and the correlation of age related hearing loss was discussed. Finally, the electrophysiological method of patch clamp was used to use Tyr. Phostina23 (tyrosine phosphorylation inhibitor A23) inhibits the cohesive function of AP-2 protein and affects the endocytosis of CME. The possible mechanism of AP-2 protein in the cochlear IHC synaptic vesicle swallowing is preliminarily discussed by studying the specific inhibition of the IHC electrophysiology of the mouse cochlea by the specific inhibition of the AP-2 protein, so as to study the sensorineural deafness in the egg. Two, materials and methods 1, materials and methods 1, select 20 healthy adult c57bl/6j (8 weeks old) mice, the auricle is sensitive and the ABR threshold is normal. By AP-2 and DAPI double markers and AP-2, ctbp2 and DAPI three markers, the immunofluorescent labeling technique combined with laser confocal microscope to observe the cochlear capillary of AP-2 protein The location and expression of.2, 7,15,35 day, and 20 mice in 16 month old mice, respectively representing newborn mice, hearing functional development mice, hearing functional mature mice and senile mice, using immunofluorescent laser confocal microscopy, qRT-PCR technique to detect the expression of AP-2 protein in the basal membrane of the hair cells, and ABR for the determination of the mouse hearing. Threshold, etc., to discuss the occurrence, formation of auditory function, and the correlation of age related impairment of auditory function with the expression of AP-2 protein in the cochlea of mice, and the inhibition of the interaction between the yxx molecular signal and AP-2 2 subunit by tyrphostina23 (tyrosine phosphorylation inhibitor A23), and the analysis of the electrophysiological changes of IHC in the mouse after the specific inhibition of the internal capillary cell AP-2 protein. Change the situation to reflect the effect of AP-2 protein on CME. Three, results: 1, AP-2 protein belongs to cytoplasmic protein, mainly expressed in the activation site of IHC synapse, which is concentrated in the lateral of cytoplasm basement. The morphological loci of the.Ap-2 protein expression near the afferent neuron region reflect the function of CME pathway, and the ABR threshold determination is found, p15 The hearing threshold of p35,16 months of age in mice was 18.67 + 1.21dbnhl, 13.83 + 1.47dbnhl and 37.83 + 7.68dbnhl, and the hearing loss in P7 group was not elicited. The software P7, p15, p35 and 16 month old groups of fluorescent staining density values (IMV) were 190.91 + 17.27494.06 + 27.63838.41 + 38.23682.65 72.22, respectively. The amount of RQ was 0.53 + 0.09,1.03 + 0.02,1.00 + 0.09,1.03 + 0.06.p7 and p15 group respectively. With the emergence and formation of auditory function, the expression of immunofluorescence light density and ap-2mrna relative expression suggested that the expression level of AP-2 increased significantly, and the difference was statistically significant (P0.05); P35 and the 16 month old groups were compared with the fluorescent light density of the AP-2 protein in the elderly group. However, the expression level of AP-2 mRNA was analyzed by Q RT-PCR, and the difference was not statistically significant (P0.05).3. The cohesive function of AP-2 protein was hindered by the inhibition of Tyrphostin A23, and then the CME path was hindered, the IHC voltage dependent Ca2+ channel opening and closing delay, the decrease of delta, the capacitance and the calcium current were reduced. The changes indicated that the CME pathway regulated by AP-2 protein participates in the endocytosis of vesicles in the IHC synaptic region. Four, conclusion 1, AP-2 protein is mainly expressed in the IHC synaptic activation region in adult mouse cochlea. The location of the morphologic loci is in accordance with the function of the CME pathway, which reflects the Association and significance of the AP-2 protein with the synapse. It may play an important role in the endocytosis of IHC synaptic vesicles, which lays a foundation for the in-depth exploration of the role of AP-2 protein in the auditory physiology and pathology of the inner ear. The AP-2 protein has unequal intensity expression in different stages of the development of the inner ear of mice, the generation of newborn mice to hearing and the mature stage, and the AP-2 protein of the cochlea with the age of mice. The expression of AP-2 protein may be enhanced, suggesting that the expression level of the protein may be related to the occurrence of auditory function, the formation and maintenance of the closely related.3, the specific inhibition of the function of the AP-2 protein and the influence of the CME pathway. The neurotransmitters in the synaptic gap can not be effectively recovered from the IHC presynaptic membrane, which affects the synaptic cycle and ultimately affects the release of the IHC neurotransmitter. It indicates that AP-2 protein plays an important role in regulating the recovery of synaptic vesicles in mouse cochlea IHC.
【學(xué)位授予單位】：第三軍醫(yī)大學(xué)
【學(xué)位級(jí)別】：碩士
【學(xué)位授予年份】：2015
【分類號(hào)】：R764.35
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