本文關(guān)鍵詞：丙泊酚對新生小鼠大腦梨狀皮層中間神經(jīng)元的影響及相關(guān)作用研究　出處：《第三軍醫(yī)大學(xué)》2016年碩士論文　論文類型：學(xué)位論文

  更多相關(guān)文章： 丙泊酚 c-Fos 梨狀皮層 中間神經(jīng)元 神經(jīng)前體細胞 神經(jīng)行為學(xué)

【摘要】：研究背景:丙泊酚(Propofol)是一種短效的、新型快速的全身麻醉藥物,因其起效迅速、作用時間短、蘇醒快、術(shù)后惡心嘔吐發(fā)生率低而被廣泛應(yīng)用于臨床麻醉及ICU鎮(zhèn)靜。近年來,麻醉藥物對發(fā)育大腦認知、學(xué)習(xí)記憶的影響是大家關(guān)注的熱點問題。臨床研究結(jié)果表明,兩歲以下嬰幼兒全麻藥物暴露可致較長時間的人格及行為改變。然而,全麻藥物丙泊酚所致神經(jīng)毒性的機制仍不明確。大腦梨狀皮層(Piriform cortex)位于前腦腹外側(cè),源于古皮質(zhì),屬邊緣系統(tǒng),是哺乳動物最大的嗅覺皮層,接受嗅球的單突觸輸入,且與相關(guān)皮層及海馬間存在復(fù)雜的纖維投射。梨狀皮層由三層皮質(zhì)組成,第一層稱為網(wǎng)織層,主要接受外側(cè)嗅束的投射纖維,第二、三層稱為細胞層,主要接收外側(cè)嗅束、相鄰皮層的興奮輸入及局部中間神經(jīng)元的抑制傳入。發(fā)育期大腦梨狀皮層神經(jīng)前體細胞具有增殖及分化發(fā)育為成熟神經(jīng)元的能力,該皮層同海馬及室管膜下區(qū)一樣存在神經(jīng)發(fā)生的潛能。此外,梨狀皮層的細胞層主要由數(shù)量較多的釋放谷氨酸的椎體神經(jīng)元及數(shù)量較少釋放γ-氨基丁酸的中間神經(jīng)元組成。梨狀皮層的中間神經(jīng)元按其細胞表面標(biāo)記物主要分為鈣結(jié)合蛋白(PV—Parvalbumin、CB—Calbindin、CR—Calretinin)中間神經(jīng)元和神經(jīng)肽(SOM—Somatostatin、NPY—Neuropeptide Y、CCK—Cholecystokinin)中間神經(jīng)元兩大類。該皮層內(nèi)上述中間神經(jīng)元的功能頗為復(fù)雜,涉及樹突的傳入、軸突的輸出以及各中間神經(jīng)元的遠程聯(lián)接。正是因為對信息傳入、輸出的調(diào)控,該區(qū)域內(nèi)的中間神經(jīng)元在嗅覺的學(xué)習(xí)、記憶過程中起重要作用。既往研究發(fā)現(xiàn),對阿爾茨海默病(Alzheimer’s disease,AD)患者而言,其嗅覺損害癥狀早于認知障礙的發(fā)生,并且其大腦梨狀皮層SOM及CR中間神經(jīng)元與AD病理性標(biāo)記物β-淀粉樣蛋白(Amyloidβ,Aβ)及Tau蛋白之間存在共同標(biāo)記,這提示梨狀皮層中間神經(jīng)元在AD的發(fā)生及發(fā)展中的易損性及其與認知障礙的密切相關(guān)性。此外,多項研究證實,尿烷(Urethane)麻醉可導(dǎo)致大腦梨狀皮層選擇性的中間神經(jīng)元損傷,這可能與麻醉所致的認知功能損害相關(guān)。換而言之,梨狀皮層可能是麻醉藥物發(fā)揮其神經(jīng)毒性作用新的靶區(qū)。神經(jīng)行為障礙(neurobehavioraldisorders)是由多種與大腦疾病或損傷相關(guān)聯(lián)的行為功能損害組成。神經(jīng)行為學(xué)(neuroethology)則是對動物的行為及神經(jīng)系統(tǒng)機制研究的方法,目的是通過動物的特殊行為學(xué)改變了解中樞神經(jīng)系統(tǒng)(centralnervoussystem,cns)病變。既往研究表明,新生期吸入麻醉藥七氟烷暴露不僅引發(fā)學(xué)習(xí)認知功能受損,還可導(dǎo)致類似自閉癥樣的社交行為學(xué)異常。結(jié)合本課題組前期研究成果:丙泊酚抑制發(fā)育大腦海馬齒狀回神經(jīng)干細胞的增殖,進一步探究丙泊酚對認知相關(guān)行為的影響及其可能的機制。研究方法:本課題首先采用出生后7天(postnatal7,p7)的新生小鼠進行丙泊酚(30mg/kg組及60mg/kg組)或脂肪乳腹腔注射以建立丙泊酚模型,應(yīng)用c-fos免疫組織化學(xué)染色方法篩選丙泊酚對發(fā)育大腦的激活靶區(qū)及定性該靶區(qū)內(nèi)易損神經(jīng)元的類別;同樣地,采用免疫組織化學(xué)方法檢測丙泊酚激活區(qū)域(梨狀皮層)神經(jīng)前體細胞增殖以明確丙泊酚對發(fā)育大腦梨狀皮層神經(jīng)發(fā)生的影響。此外,建立丙泊酚多次注射模型,即p7-p9連續(xù)注射丙泊酚并飼養(yǎng)至成年以觀察發(fā)育期丙泊酚暴露對遠期神經(jīng)行為的影響。采用食物埋藏實驗(buriedfoodtest)檢測丙泊酚模型小鼠與對照組小鼠的嗅覺識別及嗅覺學(xué)習(xí)記憶功能;采用社交實驗(sociabilityandpreferencefornoveltytest)檢測丙泊酚模型小鼠與對照組小鼠的社會行為及社會偏好;采用新物體識別實驗(novelobjectrecognitiontest)檢測丙泊酚模型小鼠與對照組小鼠的認知記憶功能。最后,應(yīng)用免疫組織化學(xué)方法檢測p21小鼠大腦梨狀皮層易損神經(jīng)元的改變以探討丙泊酚影響發(fā)育大腦神經(jīng)行為可能的機制。研究結(jié)果:1、丙泊酚激活發(fā)育大腦梨狀皮層中間神經(jīng)元(1)c-fos免疫組織化學(xué)結(jié)果表明:與脂肪乳對照組小鼠相比,丙泊酚30mg/kg組(p0.05)及丙泊酚60mg/kg組(p0.05)小鼠大腦梨狀皮層c-fos+細胞均顯著增多。(2)c-fos與neun及gfap雙重標(biāo)記免疫組織化學(xué)結(jié)果表明:三組間,neun標(biāo)記的成熟神經(jīng)元數(shù)量無差異;丙泊酚30mg/kg組及丙泊酚60mg/kg組與脂肪乳對照組相比c-fos與neun雙重標(biāo)記陽性細胞數(shù)量均顯著增多(p0.05);然而,c-fos與gfap無共標(biāo)陽性細胞。(3)c-fos與cb、cr、som、npy雙重標(biāo)記免疫組織化學(xué)結(jié)果表明:丙泊酚30mg/kg組及丙泊酚60mg/kg組與脂肪乳對照組相比c-fos與cb雙重標(biāo)記陽性細胞數(shù)量均顯著增多(p0.01);然而,c-fos與cr中神經(jīng)元及神經(jīng)肽類中間神經(jīng)元標(biāo)記物som、npy之間幾乎沒有共標(biāo)陽性細胞。2、丙泊酚對發(fā)育大腦梨狀皮層神經(jīng)前體細胞增殖的影響(1)brdu免疫組織化學(xué)結(jié)果表明:與脂肪乳對照組小鼠相比,丙泊酚30mg/kg組(p0.05)及丙泊酚60mg/kg組(p0.01)小鼠大腦梨狀皮層brdu+細胞均顯著減少;且與丙泊酚30mg/kg組相比,丙泊酚60mg/kg組小鼠大腦梨狀皮層brdu+細胞減少更為顯著(p0.05)。(2)sox2與brdu雙重標(biāo)記免疫組織化學(xué)結(jié)果表明:與脂肪乳對照組小鼠相比,丙泊酚30mg/kg組小鼠大腦梨狀皮層sox2+細胞無顯著差異,丙泊酚60mg/kg組小鼠大腦梨狀皮層sox2+細胞則減少顯著(p0.01)。同樣地,brdu-sox2雙標(biāo)陽性細胞數(shù)量丙泊酚30mg/kg組與脂肪乳對照組相比,改變無顯著差異,而丙泊酚60mg/kg組則顯著減少(p0.01)。(3)nestin免疫組織化學(xué)結(jié)果表明:與脂肪乳對照組小鼠相比,丙泊酚30mg/kg組及丙泊酚60mg/kg組小鼠大腦梨狀皮層nestin標(biāo)記神經(jīng)干細胞纖維突起分布稀疏且排列紊亂(p0.01)。3、發(fā)育期丙泊酚麻醉暴露對成年期神經(jīng)行為學(xué)的影響及可能機制(1)食物埋藏實驗結(jié)果表明:丙泊酚30mg/kg組小鼠與對照組小鼠相比探索埋藏食物的潛伏期無明顯改變,然而丙泊酚60mg/kg組小鼠與對照組及丙泊酚30mg/kg組小鼠相比,探索埋藏食物的潛伏期則明顯增加(p0.01,p0.05)。(2)社交實驗結(jié)果表明:對照組小鼠較喜歡呆在有小鼠的一側(cè)箱體(p0.05),而丙泊酚30mg/kg組及丙泊酚60mg/kg組小鼠在兩側(cè)箱體的時間則無差異;在該實驗的第二階段即社會新奇偏好性測試中,對照組小鼠較偏好與陌生小鼠交流(p0.01),而丙泊酚30mg/kg組及丙泊酚60mg/kg組小鼠則未有如此表現(xiàn)。(3)新物體識別實驗結(jié)果表明:對照組小鼠新物體的探索時間較舊物體探索時間明顯增多(p0.001),而丙泊酚30mg/kg組及丙泊酚60mg/kg組小鼠則無明顯偏好性。換言之,丙泊酚30mg/kg組及丙泊酚60mg/kg組小鼠較對照組小鼠新物體分辨率明顯下降(p0.001)。(4)p21小鼠大腦切片免疫組織化學(xué)染色結(jié)果顯示,丙泊酚30mg/kg組及丙泊酚60mg/kg組小鼠大腦梨狀皮層cb中間神經(jīng)數(shù)量均顯著減少,提示梨狀皮層cb中間神經(jīng)元在發(fā)育期丙泊酚麻醉作用中表現(xiàn)出特異性地易損性。研究結(jié)論:上述研究結(jié)果提示:丙泊酚通過抑制發(fā)育大腦梨狀皮層神經(jīng)前體細胞增殖及激活該區(qū)域內(nèi)CB中間神經(jīng)元,進而影響遠期認知、學(xué)習(xí)、記憶功能。
[Abstract]:Background: Propofol (Propofol) is a short acting, all new fast narcotic drugs, because of its rapid onset, short duration, fast recovery, low incidence of postoperative nausea and vomiting have been widely used in clinical anesthesia and sedation in ICU. In recent years, anesthetics on brain development of cognition, learning and memory effect is a hot issue of concern. The clinical research results show that the change of infants under two general anesthesia drug exposure can cause a long time personality and behavior. However, the mechanism of general anesthesia of propofol induced neurotoxicity is not clear. The brain in piriform cortex (Piriform cortex) is located in the ventrolateral forebrain, originated from the ancient cortex, belongs to the limbic system, is the largest mammalian olfactory cortex, single synaptic input accept of the olfactory bulb, and there are projections associated with complex cortex and hippocampus. The piriform cortex consists of three layers of cortex, the first layer is called the net The main layer, accept projection fibers in the lateral olfactory tract, the second, third layer is a layer of cells, mainly for receiving the lateral olfactory tract, inhibition of excitatory inputs and local interneurons adjacent cortical afferent. During the development of brain in piriform cortex neural precursor cells proliferation and differentiation ability of mature neurons, in the hippocampus and cortex of the same the subventricular zone exists neurogenesis potential. In addition, interneurons in piriform cortex cell layer is mainly composed of a large number of glutamate release vertebral neurons and fewer release GABA interneurons. Pear shaped skin layer according to its cell surface markers consists of calcium binding protein (PV - Parvalbumin, CB - Calbindin, CR - Calretinin) and neuropeptide interneurons (SOM - Somatostatin, NPY - Neuropeptide Y, CCK Cholecystokinin). The two types of interneurons in the cortex. The intermediate neuron function is quite complex, involving afferent dendrites, axons and neurons of the intermediate output remote join. It is precisely because of the incoming information, output control, the area of the interneurons in the olfactory learning, plays an important role in the process of memory. Not only to study found in Alzheimer's disease (Alzheimer 's disease, AD) patients, the olfactory impairment symptoms of early cognitive dysfunction in the brain, and piriform cortex SOM and CR neurons and AD pathological markers of beta amyloid (Amyloid beta, beta A) are common markers between Tau and protein, suggesting that the close relationship between the vulnerability of piriformis cortical interneurons in the occurrence and development of AD in and cognitive disorders. In addition, a number of studies have confirmed that urethane (Urethane) anesthesia can cause brain damage among neurons in piriform cortex selectively, which may be related to Related to cognitive impairment caused by anaesthesia. In other words, the piriform cortex may be the anesthetic drug exerts its neurotoxic effects of new target areas. Neurobehavioral disorders (neurobehavioraldisorders) is composed of a variety of disease or injury related behavior and brain function damage. Combined neural behavior (neuroethology) is a method of behavior and neural mechanism Research on animal, animal behavior through special purpose is to observe the histological change of central nervous system (centralnervoussystem, CNS) disease. Previous studies showed that neonatal exposure not only caused seven halothane inhalation anesthetics learning impaired cognitive function, can also lead to similar social behavior in autism kind of abnormal. Combined with the previous research results: propofol inhibits development of hippocampus neural stem cell proliferation, to further explore the effects of propofol on cognitive behavior and The possible mechanism. Methods: firstly, using 7 days after birth (postnatal7, P7) of newborn mice were propofol (group 30mg/kg and group 60mg/kg) model was established by propofol or Intralipid intraperitoneal injection, c-fos immunohistochemistry screening of propofol on activation of target area and the qualitative target area of vulnerable neurons the categories of brain development; similarly, the detection of propofol activation region by immunohistochemical method (piriform cortex) affect the proliferation of neural precursor cells to determine propofol on brain development in piriform cortex neurogenesis. In addition, the establishment of multiple propofol injection model, namely p7-p9 continuous injection of propofol and reared to adulthood in order to observe the development of propofol effects of exposure on neurobehavioral food. The burial experiment (buriedfoodtest) detection of propofol and the control group of mice model mice olfactory recognition and olfactory Feel the learning and memory function; the social experiment (sociabilityandpreferencefornoveltytest) detection model mice and control mice with social behavior and social preference; the new object recognition test (novelobjectrecognitiontest) detection of propofol mice and control mice cognitive memory function. Finally, the mechanism of immunohistochemical detection of p21 mouse brain piriform cortex in vulnerable neurons in order to investigate the effect of propofol may change the development of brain behavior. Results: 1, the development of brain activation of propofol in piriform cortex neurons (1) c-fos immunohistochemistry results showed that compared with fat emulsion group mice, propofol 30mg/kg group (P0.05) and propofol group (60mg/kg P0.05) in brain of mouse piriform cortex c-fos+ the cells were significantly increased. (2) c-fos and NeuN and GFAP double labeling immunohistochemistry results showed that Between three groups, no difference in the number of mature neurons labeled with NeuN; group 30mg/kg propofol and propofol 60mg/kg group and control group compared to the number of fat emulsion c-fos and NeuN double labeled positive cells were significantly increased (P0.05); however, c-fos and GFAP were labeled positive cells. (3) c-fos and CB, Cr, SOM. NPY double labeling immunohistochemistry results showed that propofol 30mg/kg group and propofol group 60mg/kg with fat emulsion group compared to the number of c-fos and CB double labeled positive cells were significantly increased (P0.01); however, c-fos and Cr in neurons and neuropeptides in neuronal markers SOM, NPY almost no labeled.2 positive cells. Effect of propofol on brain development in piriform cortex the proliferation of neural precursor cells (1) BrdU immunohistochemistry results showed that compared with fat emulsion group mice, propofol 30mg/kg group (P0.05) and propofol group (60mg/kg P0.01) in mouse brain The piriform cortex brdu+ cells were significantly reduced; compared with propofol 30mg/kg group, propofol group 60mg/kg mice brain piriform cortex brdu+ cells reduced significantly (P0.05). (2) Sox2 and BrdU double labeling immunohistochemistry results showed that compared with the fat milk control mice, there was no significant difference between the propofol group 30mg/kg mice brain the piriform cortex sox2+ cells, propofol group 60mg/kg mice brain piriform cortex of sox2+ cells decreased significantly (P0.01). Similarly, the number of brdu-sox2 positive cells in group 30mg/kg propofol and Intralipid were compared with the control group, no significant difference in change, and propofol 60mg/kg group decreased significantly (P0.01). (3) nestin immunohistochemistry the results showed that: compared with chemical fat emulsion group mice, propofol 30mg/kg group and propofol group 60mg/kg mice brain piriform cortex nestin neural stem cells labeled fibers projecting sparse and arranged orderly Chaos (P0.01).3, during the development of propofol exposure on the neurobehavioral effects of adult learning and the possible mechanism of buried food (1) the experimental results show that the propofol 30mg/kg group mice compared with control mice had no obvious change in the exploration of buried food latency, however compared with propofol 60mg/kg group with the control group and propofol group 30mg/kg mice. Exploration of buried food latency increased significantly (P0.01, P0.05). (2) social experiment results showed that the control group of mice than love stay in the side box with the mouse (P0.05), and the time on both sides of the box of propofol 30mg/kg group and propofol group 60mg/kg mice had no significant difference; in the second phase of the experiment that the social novelty preference test, the mice of control group were unfamiliar with the preference of mice (P0.01), and the exchange of propofol 30mg/kg group and propofol group 60mg/kg mice were not so. (3) a new object recognition experiment The results showed that the mice of control group new object of exploration time than the old object exploration time increased significantly (p0.001), and propofol 30mg/kg group and propofol group 60mg/kg mice had no obvious preference. In other words, propofol group 30mg/kg and propofol in 60mg/kg group decreased significantly compared with the control group of mice (p0.001). The new resolution (4 p21 mouse brain slices) immunohistochemical staining showed that the number of propofol 30mg/kg group and propofol group 60mg/kg mice brain piriform cortex CB intermediate nerve were significantly reduced, suggesting that showing vulnerability specific piriform cortex CB interneurons in the development period of anesthetic action of propofol. Conclusions: the results suggest that propofol by inhibiting the development of brain nerve anterior piriform cortex and the region of CB interneurons activated cell proliferation, thereby affecting the long-term cognitive, learning, and memory.

【學(xué)位授予單位】：第三軍醫(yī)大學(xué)
【學(xué)位級別】：碩士
【學(xué)位授予年份】：2016
【分類號】：R614

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