本文選題：癲癇　切入點(diǎn)：酪氨酸激酶受體B　出處：《天津醫(yī)科大學(xué)》2016年博士論文　論文類(lèi)型：學(xué)位論文

【摘要】：研究目的:Micro RNA(mi RNA)是一類(lèi)內(nèi)源性小分子非編碼RNA,作為轉(zhuǎn)錄后調(diào)控因子,參與癲癇發(fā)病機(jī)制的多個(gè)蛋白編碼基因的表達(dá)。腦源性神經(jīng)營(yíng)養(yǎng)因子(brain-derived neurotrophic factor,BDNF)-酪氨酸激酶受體B(tropomyosin-related kinase receptor type B,Trk B)信號(hào)通路是癲癇發(fā)生的關(guān)鍵通路,選擇性中樞神經(jīng)系統(tǒng)內(nèi)敲除Trk B基因能完全阻止點(diǎn)燃誘發(fā)的癲癇發(fā)作。有關(guān)研究發(fā)現(xiàn)mi R-204-5p(mi R-204)能通過(guò)調(diào)控Trk B受體影響腫瘤的發(fā)生和轉(zhuǎn)移,深入研究mi R-204是否能通過(guò)Trk B信號(hào)通路調(diào)控癲癇的發(fā)生,有望為臨床癲癇治療提供新的思路。根據(jù)上述研究背景提出本論文的研究目的如下:1.以原代培養(yǎng)的大鼠海馬神經(jīng)元的癇樣放電模型為研究對(duì)象,通過(guò)Trk B受體及其下游信號(hào)通路,研究mi R-204抑制神經(jīng)元癇樣放電和電壓門(mén)控性Ca2+通道(voltage-gated calcium channel,VGCC)電流的機(jī)制。2.在mi R-204抑制神經(jīng)元癇樣放電的研究基礎(chǔ)上,選取前期研究的在癲癇神經(jīng)元模型中異常表達(dá)并且與BDNF-Trk B通路相關(guān)的mi R-132-3p(mi R-132)為靶點(diǎn),研究過(guò)表達(dá)mi R-132后神經(jīng)元癇樣放電和VGCC電流的改變,為探索其他類(lèi)型mi Rs在癲癇發(fā)病機(jī)制中的作用提供創(chuàng)新思路與方法。研究方法:1.原代培養(yǎng)的海馬神經(jīng)元經(jīng)無(wú)鎂細(xì)胞外液處理3h,建立神經(jīng)元癇樣放電模型。2.Mi R-204調(diào)控Trk B信號(hào)通路抑制神經(jīng)元癇樣放電的機(jī)制研究。(1)通過(guò)實(shí)時(shí)熒光定量PCR(real-time quantitative polymerase chain reaction,q RT-PCR)檢測(cè)神經(jīng)元癇樣放電模型中mi R-204的表達(dá)改變。(2)應(yīng)用包含mi R-204-p GLVH1/GFP的慢病毒載體轉(zhuǎn)染原代培養(yǎng)的海馬神經(jīng)元以過(guò)表達(dá)mi R-204,通過(guò)q RT-PCR檢測(cè)過(guò)表達(dá)mi R-204后Trk B m RNA的表達(dá)改變。(3)Trk B下游通路的代表性信號(hào)分子包括Akt,PLCγ1,ERK1/2和CREB。通過(guò)western blotting以這些信號(hào)分子的磷酸化蛋白水平和總蛋白水平的比值反映信號(hào)分子的激活程度,研究神經(jīng)元癇樣放電模型模型中mi R-204調(diào)控Trk B下游信號(hào)分子活性的相關(guān)機(jī)制。(4)應(yīng)用全細(xì)胞膜片鉗電流鉗技術(shù)檢測(cè)神經(jīng)元癇樣放電模型的放電特性,神經(jīng)元癇樣放電模型過(guò)表達(dá)mi R-204后檢測(cè)癇樣放電頻率的變化。(5)應(yīng)用全細(xì)胞膜片鉗電壓鉗技術(shù)檢測(cè)神經(jīng)元癇樣放電模型VGCC電流和穩(wěn)態(tài)激活與失活特性的變化,神經(jīng)元癇樣放電模型過(guò)表達(dá)mi R-204后VGCC特性的改變。3.Mi R-132調(diào)控BDNF影響神經(jīng)元癇樣放電的機(jī)制研究。為研究其他mi Rs在癲癇發(fā)病機(jī)制中的作用是否一致,選取前期研究發(fā)現(xiàn)在神經(jīng)元癇樣放電模型中表達(dá)上調(diào)的mi R-132為靶點(diǎn),研究mi R-132對(duì)神經(jīng)元癇樣放電和VGCC電流的調(diào)控,并進(jìn)一步探討其調(diào)控機(jī)制。(1)通過(guò)q RT-PCR檢測(cè)神經(jīng)元癇樣放電模型中BDNF m RNA的表達(dá),慢病毒轉(zhuǎn)染過(guò)表達(dá)mi R-132后觀察BDNF m RNA的表達(dá)改變,研究mi R-132調(diào)控BDNF表達(dá)的機(jī)制。(2)應(yīng)用全細(xì)胞膜片鉗電流鉗技術(shù)檢測(cè)神經(jīng)元癇樣放電模型分別過(guò)表達(dá)mi R-132和孵育外源性BDNF后癇樣放電頻率的變化。(3)應(yīng)用全細(xì)胞膜片鉗電壓鉗技術(shù)檢測(cè)神經(jīng)元癇樣放電模型分別過(guò)表達(dá)mi R-132和孵育外源性BDNF后VGCC電流特性的改變。研究結(jié)果:1.Mi R-204調(diào)控Trk B信號(hào)通路抑制神經(jīng)元癇樣放電。(1)神經(jīng)元癇樣放電模型中mi R-204的表達(dá)下調(diào):與正常對(duì)照組神經(jīng)元相比,癲癇模型組中mi R-204的表達(dá)水平明顯下降(P0.001,n=6)。(2)Mi R-204負(fù)調(diào)控Trk B受體m RNA的表達(dá):Trk B m RNA的表達(dá)水平在癲癇模型組和對(duì)照組無(wú)明顯差異(P0.05,n=6)。癲癇模型組過(guò)表達(dá)mi R-204后Trk B m RNA表達(dá)明顯降低(P0.001,n=6)。(3)Mi R-204抑制Trk B受體下游信號(hào)通路的活性:神經(jīng)元癇樣放電模型中Akt信號(hào)通路活性無(wú)明顯改變,PLCγ1(P0.001,n=6)、ERK1/2(P0.001,n=6)以及CREB(P0.001,n=6)信號(hào)活性均明顯增強(qiáng)。在神經(jīng)元癇樣放電模型中過(guò)表達(dá)mi R-204后PLCγ1信號(hào)活性無(wú)明顯改變(P0.05,n=6),而ERK1/2信號(hào)活性(P0.01,n=6)以及CREB信號(hào)活性(P0.001,n=6)均明顯降低。證明mi R-204主要調(diào)控Trk B受體下游的ERK1/2-CREB信號(hào)通路。(4)Mi R-204抑制神經(jīng)元的癇樣放電:全細(xì)胞電流鉗檢測(cè)正常對(duì)照神經(jīng)元表現(xiàn)為偶發(fā)的動(dòng)作電位發(fā)放;而癲癇模型組表現(xiàn)為持續(xù)高頻的動(dòng)作電位發(fā)放,放電頻率比正常對(duì)照組明顯增高(P0.001,n=14)。癲癇模型組過(guò)表達(dá)mi R-204后神經(jīng)元的癇樣放電頻率明顯降低(P0.001,n=14)。(5)Mi R-204抑制神經(jīng)元癇樣放電模型中神經(jīng)元VGCC電流和活性:神經(jīng)元癇樣放電模型VGCC的最大電流密度增加(P0.001,n=10),穩(wěn)態(tài)激活曲線(xiàn)的半數(shù)激活電壓降低(P0.01,n=10),穩(wěn)態(tài)失活曲線(xiàn)的半數(shù)失活電壓升高(P0.01,n=10),表明神經(jīng)元癇樣放電模型VGCC電流增強(qiáng),通道更易激活難以失活。神經(jīng)元癇樣放電模型過(guò)表達(dá)mi R-204后,最大電流密度降低(P0.001,n=10),穩(wěn)態(tài)激活曲線(xiàn)的半數(shù)激活電壓增高(P0.05,n=10),穩(wěn)態(tài)失活曲線(xiàn)的半數(shù)失活電壓降低(P0.01,n=10),說(shuō)明mi R-204抑制神經(jīng)元癇樣放電模型中神經(jīng)元的VGCC電流和活性。2.神經(jīng)元癇樣放電模型中mi R-132抑制BDNF加重癇樣放電。(1)在神經(jīng)元癇樣放電模型中mi R-132抑制BDNF m RNA的表達(dá):癲癇模型中BDNF m RNA的表達(dá)水平明顯上調(diào)(P0.001,n=6)。對(duì)照神經(jīng)元過(guò)表達(dá)mi R-132后BDNF m RNA的表達(dá)水平明顯增高(P0.001,n=6),而神經(jīng)元癇樣放電模型過(guò)表達(dá)mi R-132后BDNF m RNA的表達(dá)水平明顯下降(P0.001,n=6)。(2)BDNF抑制神經(jīng)元癇樣放電,而mi R-132逆轉(zhuǎn)這一作用加重神經(jīng)元癇樣放電:癲癇模型組過(guò)表達(dá)mi R-132后放電頻率明顯增高(P0.01,n=14)。癲癇模型組孵育BDNF后放電頻率明顯降低(P0.001,n=14),但在此基礎(chǔ)上過(guò)表達(dá)mi R-132后放電頻率又增高到癲癇模型組水平(Mg2+-free+BDNF+mi R-132:Mg2+-free=7.11±2.90:6.54±2.64,P0.5,n=14)。說(shuō)明BDNF對(duì)神經(jīng)元癇樣放電有抑制作用,而在mi R-132過(guò)表達(dá)時(shí)這種抑制作用消失,mi R-132能明顯加重神經(jīng)元癇樣放電。(3)BDNF抑制癇樣放電神經(jīng)元VGCC電流和活性,而mi R-132能逆轉(zhuǎn)這一作用加重VGCC電流和活性:癲癇模型組過(guò)表達(dá)mi R-132后VGCC最大電流密度增加(P0.01,n=10)。癲癇模型組孵育BDNF后VGCC最大電流密度降低(P0.05,n=10),穩(wěn)態(tài)激活曲線(xiàn)的半數(shù)激活電壓增高(P0.001,n=10),穩(wěn)態(tài)失活曲線(xiàn)的半數(shù)失活電壓降低(P0.01,n=10),但在此基礎(chǔ)上過(guò)表達(dá)mi R-132后逆轉(zhuǎn)了VGCC特性的改變。說(shuō)明BDNF對(duì)癇樣放電神經(jīng)元增強(qiáng)的VGCC有抑制作用,而mi R-132則相反加強(qiáng)癇樣放電神經(jīng)元VGCC的電流和活性。結(jié)論:1.Mi R-204調(diào)控Trk B信號(hào)通路抑制神經(jīng)元癇樣放電。(1)神經(jīng)元癇樣放電模型中mi R-204的表達(dá)下調(diào)。(2)Mi R-204抑制Trk B m RNA的表達(dá)。(3)在神經(jīng)元癇樣放電模型中Trk B下游信號(hào)通路PLCγ1和ERK1/2-CREB激活,而其中ERK1/2-CREB信號(hào)通路的激活能被mi R-204抑制。(4)Mi R-204抑制神經(jīng)元癇樣放電模型的癇樣放電和VGCC電流。2.Mi R-132抑制BDNF加重神經(jīng)元癇樣放電。(1)在神經(jīng)元癇樣放電模型中mi R-132抑制BDNF m RNA的表達(dá)。(2)BDNF抑制神經(jīng)元癇樣放電和VGCC電流活性,而mi R-132能逆轉(zhuǎn)這一作用加重神經(jīng)元癇樣放電和加強(qiáng)VGCC電流活性。
[Abstract]:Objective: Micro RNA (MI RNA) is a class of endogenous small molecule non encoding RNA, as a factor regulating transcription, expression of multiple genes encoding proteins involved in the pathogenesis of epilepsy. Brain derived neurotrophic factor (brain-derived neurotrophic, factor, BDNF) - tyrosine kinase receptor B (tropomyosin-related kinase receptor type B. Trk B) signaling pathway is a key of epilepsy, selective central nervous system Trk B gene knockout can completely prevent the kindling induced seizures. The study found that MI R-204-5p (MI R-204) can be affected by the regulation of Trk B receptor in tumor progression and metastasis, in-depth study of MI R-204 is Trk through B signaling pathway the regulation of the occurrence of epilepsy, is expected to provide new ideas for clinical treatment of epilepsy. According to the above research objective of this dissertation was put forward as follows: 1. rat hippocampal neurons in primary culture The epileptiform discharge model element as the research object, through the Trk B receptor and its downstream signaling pathways, inhibition of neuronal epileptiform discharges and voltage-gated Ca2+ channels of MI R-204 (voltage-gated calcium channel, VGCC) based on the mechanism of.2. current in MI R-204 inhibits neuronal epileptiform discharge on the selection of the previous studies in epileptic neuron the model and associated with the abnormal expression of BDNF-Trk B mi R-132-3p (MI R-132 pathway) as the target, studied the changes of neurons epileptiform discharge and VGCC current expression of MI R-132, provides a new idea and method for exploring the role of other types of MI Rs in the pathogenesis of epilepsy. Methods: hippocampal neurons after 3H liquid magnesium free cell culture 1. primary, establish mechanism of epileptiform discharges of neuron model.2.Mi R-204 control Trk B signal pathway and inhibition of neuronal epileptiform discharges (1) by real-time fluorescence. Light PCR (real-time quantitative polymerase chain quantitative reaction, Q RT-PCR) to change the expression of epileptiform discharges of neuron model in MI R-204. (2) lentiviral vector containing mi R-204-p GLVH1/GFP transfection in primary cultured hippocampal neurons by overexpression of MI R-204, by Q RT-PCR detection expression of MI R-204 changed after Trk B m RNA. (3) the representative signal molecule Trk B downstream pathways including Akt, PLC ERK1/2 and CREB. gamma 1, the ratio of the total protein level and phosphorylated protein levels of these molecules reflect the degree of activation of signal molecules by Western blotting, the related mechanism of epileptiform discharges of neuron model in MI R-204 the regulation of Trk B downstream signal molecular activity. (4) the discharge characteristics using the whole cell patch clamp current clamp technique to detect neuronal epileptiform discharge model, epileptiform discharges of neuron model over expression of MI R-204 After the change detection of epileptiform discharges. (5) change and inactivation activation using the whole cell patch clamp voltage clamp technique to detect neuronal epileptiform discharge model of VGCC current and steady state, the change of.3.Mi R-132 regulatory mechanism of BDNF neurons epileptiform discharges of neurons epileptiform discharge model VGCC characteristic expression of MI after R-204. In order to investigate the role of other mi Rs in the pathogenesis of epilepsy is consistent, from previous study found that upregulation of MI R-132 expression as a target in neuronal epileptiform discharge model, MI R-132 control on epileptiform discharges of neuron and VGCC currents, and further explore its mechanism. (1) the expression of Q RT-PCR detection epileptiform discharges of neuron model with BDNF m RNA, lentivirus overexpression of MI R-132 BDNF m to observe the expression change of RNA, to study the mechanism of MI regulation of R-132 BDNF expression. (2) using the whole cell patch Detection of epileptiform discharges of neuron model clamp current clamp technique respectively the expression changes of discharge frequency of epileptiform mi R-132 and incubated with exogenous BDNF. (3) used to detect neuronal epileptiform discharge model of whole cell patch clamp technique respectively the change of expression of VGCC R-132 and current characteristics of MI incubated with exogenous BDNF. Results: 1.Mi R-204 regulation of Trk B signaling pathway inhibits neuronal epileptiform discharge. (1) expression of epileptiform discharges of neuron model in MI R-204: compared with the normal control group of neurons, the expression level of MI R-204 in epileptic model group decreased significantly (P0.001, n=6). (2) the expression of Mi R-204 Trk B negative regulation M receptor RNA: there was no significant difference in the expression level of Trk B m RNA in epilepsy model group and the control group (P0.05, n=6). The epilepsy model group expression of MI R-204 Trk B m RNA expression decreased significantly (P0.001, n=6). (3) Mi R-204 Trk inhibits B receptor downstream Pathway: Akt pathway activity of epileptiform discharges of neuron in the model did not change significantly, PLC gamma 1 (P0.001, n=6), ERK1/2 (P0.001, n=6) and CREB (P0.001, n=6) activity was significantly enhanced. The epileptiform discharges of neuron model of overexpression of MI in R-204 after PLC gamma 1 signal activity no significant change (P0.05, n=6), and ERK1/2 (P0.01, n=6) activity and CREB activity (P0.001, n=6) were significantly decreased. The results showed that ERK1/2-CREB signaling pathway downstream of MI R-204 regulatory Trk B receptor. Mi (4) R-204 inhibits epileptiform discharges of neurons: whole cell current clamp detection control neurons showed spike and occasional; epilepsy model group showed sustained spike frequency, the discharge frequency was significantly higher than the normal control group (P0.001, n=14). The epilepsy model group expression of MI R-204 after the epileptiform discharges of neurons decreased significantly (P0.0 01, n=14). (5) Mi R-204 inhibits neuronal VGCC currents and epileptiform discharges of neuron activity in the model: the maximum current density of epileptiform discharges of neuron model of VGCC (P0.001, n=10) increase, half of the steady-state activation curve of the activation voltage decreased (P0.01, n=10), half of the steady-state inactivation curve of inactivation voltage rise (P0.01, n=10), showed epileptiform discharges of neuron model VGCC current enhancement, more difficult to activate channel inactivation. Epileptiform discharges of neuron model over expression of MI R-204, the maximum current density decreased (P0.001, n=10), half of the steady-state activation curve of the activation voltage increased (P0.05, n=10), half of the steady-state inactivation curve the inactivation of voltage drop (P0.01, n=10), VGCC current and the activity of.2. neurons epileptiform discharge model mi R-204 inhibitory neurons epileptiform discharge model in MI R-132 inhibited BDNF aggravate epileptiform discharges. (1) in neuronal epileptiform discharge model in MI R-1 The expression of M RNA: 32 inhibition of BDNF was significantly up-regulated in BDNF m RNA epilepsy model (P0.001, n=6). The control over the expression level of BDNF m RNA neurons significantly increased the expression of MI R-132 (P0.001, n=6), and the epileptiform discharges of neuron model over expression of MI R-132 expression level of BDNF RNA was m decreased (P0.001, n=6). (2) BDNF inhibits epileptiform discharges of neuron, and the role of MI R-132 reversal aggravating neuronal epileptiform discharges: epilepsy model group expression of MI R-132 after the discharge frequency increased significantly (P0.01, n=14). The epilepsy model group after BDNF incubation and discharge frequency was significantly reduced (P0.001, n=14), but on the basis of over expression of MI R-132 after discharge frequency increased to the level of epilepsy model group (Mg2+-free+BDNF+mi R-132:Mg2+-free=7.11 + 2.90:6.54 + 2.64, P0.5, n=14). The results showed that BDNF had inhibitory effects on neuronal epileptiform discharge, while overexpression of MI R-132 when this suppression Mi R-132 effect disappeared, can aggravate epileptiform discharges of neuron. (3) BDNF inhibits epileptiform discharges of neurons in VGCC and MI and the current activity, R-132 can reverse the effects of increased VGCC current and activity: the epilepsy model group expression of MI R-132 VGCC the maximum current density increased (P0.01, n =10). The epilepsy model group incubation of VGCC the maximum current density decreased after BDNF (P0.05, n=10), half of the steady-state activation curve of the activation voltage increased (P0.001, n=10), half of the steady-state inactivation curve of inactivation voltage (P0.01, n=10) decreased, but based on the expression of MI R-132 after the reversal of the VGCC characteristics of the BDNF on the change. Epileptiform discharges of neurons enhanced the inhibitory effect of VGCC, MI and R-132 on the contrary strengthen current and activity of epileptiform discharges of neurons in VGCC. Conclusion: 1.Mi R-204 regulation of Trk B signaling pathway inhibits neuronal epileptiform discharge. (1) epileptiform discharges of neuron model mi R-204 table Reach down. (2) the expression of Mi R-204 B m RNA. The inhibition of Trk (3) in epileptiform discharges of neuron model Trk B signaling pathways downstream of PLC gamma 1 and ERK1/2-CREB activation, and the activation of ERK1/2-CREB signaling pathway can be inhibited. Mi R-204 (4).2.Mi epileptiform discharge and VGCC current R-132 Mi R-204 inhibition of neuronal epileptiform discharge model of inhibition of BDNF aggravate neuronal epileptiform discharge. (1) expression in neurons of epileptic discharge in the model of MI R-132 m RNA. The inhibition of BDNF (2) BDNF inhibits epileptiform discharges of neuron and VGCC current and MI activity, R-132 can reverse the effects of increased neuron epileptiform discharges and strengthening VGCC current activity.

【學(xué)位授予單位】：天津醫(yī)科大學(xué)
【學(xué)位級(jí)別】：博士
【學(xué)位授予年份】：2016
【分類(lèi)號(hào)】：R742.1

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