小鼠海馬CA1區(qū)軸棘突觸相關(guān)特性的研究
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本文關(guān)鍵詞:小鼠海馬CA1區(qū)軸棘突觸相關(guān)特性的研究 出處:《河北醫(yī)科大學(xué)》2006年博士論文 論文類(lèi)型:學(xué)位論文
更多相關(guān)文章: 軸棘突觸 樹(shù)突棘 突觸后致密體 C57BL/6小鼠 海馬 老年 FMR1-KO鼠 mGluR5
【摘要】: 在19世紀(jì)末,Ramon y Cajal首次提出典型樹(shù)突棘由與樹(shù)突相連的頸部和膨大的頭部組成,并且提到這些位于眾多神經(jīng)元樹(shù)突表面的微小突起是神經(jīng)元之間相互作用的場(chǎng)所,認(rèn)為樹(shù)突棘形態(tài)的改變可能會(huì)引起神經(jīng)元功能活動(dòng)的變化。一個(gè)世紀(jì)以來(lái),人們運(yùn)用光鏡和電鏡技術(shù)證實(shí),樹(shù)突棘的確是突觸信號(hào)輸入的裝置,在人類(lèi)的大腦中含量超出1013,參與90%以上興奮性突觸的信息傳遞,是軸棘突觸的重要結(jié)構(gòu)。軸棘突觸的樹(shù)突棘頭存在高電子密度的盤(pán)狀結(jié)構(gòu),稱(chēng)為突觸后致密體(PSD),鑲嵌著許多重要的神經(jīng)遞/調(diào)質(zhì)受體,在神經(jīng)遞/調(diào)質(zhì)信號(hào)傳遞過(guò)程中起著重要作用。樹(shù)突棘的數(shù)量或形態(tài)與突觸的效能密切相關(guān),當(dāng)其發(fā)生改變時(shí),暗示軸棘突觸也出現(xiàn)了變化,因此,可以用指定區(qū)域內(nèi)樹(shù)突棘的密度與形態(tài)特征來(lái)表示此區(qū)域內(nèi)突觸的數(shù)量和狀態(tài)。 眾所周知,海馬CA1區(qū)與空間學(xué)習(xí)記憶密切相關(guān),然而研究發(fā)現(xiàn),學(xué)習(xí)記憶減退的衰老大鼠和小鼠齒狀回顆粒細(xì)胞、海馬CA1以及海馬CA3區(qū)的錐體細(xì)胞并無(wú)神經(jīng)元數(shù)目的減少,因此,衰老引起的學(xué)習(xí)記憶減退的形態(tài)基礎(chǔ)很可能是神經(jīng)元更微細(xì)的結(jié)構(gòu)如軸棘突觸的改變。 脆性X綜合癥(FRX, fragile x syndrome)是常見(jiàn)的遺傳性智力發(fā)育遲緩疾病,其發(fā)病率為男性1/4000,女性1/8000,僅次于Down’s綜合癥。這種疾病主要是由于FMR1基因5`末端CGG重復(fù)序列增加過(guò)多,導(dǎo)致其編碼蛋白(FMRP)的表達(dá)缺乏。FRX小鼠模型是靶向破壞野生型小鼠的FMR1基因而建立,并具有其許多FRX患者的特征。FRX患者與FMR1基因敲除小鼠均表現(xiàn)有空間學(xué)習(xí)記憶障礙,暗示極有可能存在海馬錐體細(xì)胞的樹(shù)突棘和軸棘突觸的形態(tài)異常。 因此,我們通過(guò)研究正常小鼠、老年小鼠和FMR1基因敲除鼠海馬CA1區(qū)軸棘突觸的相關(guān)特性及其變化,為樹(shù)突棘或軸棘突觸參與衰老引起的學(xué)習(xí)記憶減退及FRX智力障礙提供神經(jīng)解剖學(xué)依據(jù)。研究?jī)?nèi)容如下: 一、小鼠海馬CA1區(qū)軸棘突觸樹(shù)突棘頭與突觸后致密體的相關(guān)性研究 目的:樹(shù)突棘與突觸后致密體(PSD)是軸棘突觸的重要結(jié)構(gòu),大的
[Abstract]:At the end of nineteenth Century, Ramon y Cajal first proposed the typical dendritic spines and dendrites connected by the neck and swollen head. At the end of the numerous small protrusions of neuronal dendrites is interaction between neurons where that dendritic spine morphology changes may lead to changes in the activity of neurons. For a century, people using light and electron microscopy confirmed that dendritic spines are device of synaptic input, in the human brain in excess of 1013, involved in more than 90% of excitatory synaptic transmission of information, is an important structure in axospinous synapses. There is disc structure with high electron density of dendritic spine head axospinous synapses, called synapses after the dense body (PSD), with many important neurotransmitters / neuromodulators receptors play an important role in neurotransmitter signaling process. And / or the number of dendritic spine morphology and synaptic Efficiency is closely related. When it changes, it implies that the axis spines synapse also changes. Therefore, the number and state of synapses in this area can be expressed by density and morphological characteristics of dendritic spines in designated areas.
As everyone knows, hippocampus CA1 region and spatial learning and memory are closely related, but the study found that the learning and memory of senile rats and mice granule cells in the dentate gyrus, hippocampus CA1 and CA3 region of the hippocampus pyramidal cells and no reduction in the number of neurons, therefore, learning and memory deficits caused by aging is likely to form the basis is more subtle structure of neurons if the axospinous synapses change.
Fragile X syndrome (FRX fragile, X syndrome) is a common inherited mental retardation disease, the incidence rate of male 1/4000, female 1/8000, after Down 's syndrome. This disease is mainly due to the FMR1 terminal of 5` gene CGG repeat sequence increases too much, leading to its coding protein (FMRP) expression of.FRX deficiency mouse model is targeting FMR1 gene disruption of wild-type mice and the establishment, features of.FRX patients with FMR1 gene and has many of its patients with FRX knockout mice showed spatial learning and memory disorders, suggesting that abnormal dendritic spines and axospinous synapses is likely to exist in hippocampal pyramidal cell morphology.
Therefore, we study the correlation properties in normal mice, hippocampal CA1 area axospinous synapses and changes in aged mice and FMR1 gene knock, providing neuroanatomical basis for learning and memory of dendritic spines or axospinous synapses involved in the aging caused by FRX impairment and mental retardation. The contents are as follows:
The study of the correlation between the synaptic dendrites of the synapse and the postsynaptic density in the hippocampal CA1 region of the hippocampus
Objective: dendritic spines and postsynaptic dense bodies (PSD) are important structures of axon synapses.
【學(xué)位授予單位】:河北醫(yī)科大學(xué)
【學(xué)位級(jí)別】:博士
【學(xué)位授予年份】:2006
【分類(lèi)號(hào)】:R322
【引證文獻(xiàn)】
相關(guān)碩士學(xué)位論文 前1條
1 任寶梁;應(yīng)用AMIRA軟件探討海馬CA1區(qū)軸棘突觸樹(shù)突棘與突觸后致密斑的相關(guān)性[D];河北醫(yī)科大學(xué);2013年
,本文編號(hào):1441523
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