本文選題：母體期慢性鋁暴露 + 海馬　； 參考：《中國醫(yī)科大學》2007年碩士論文

【摘要】： 母體期慢性鋁暴露對子代大鼠海馬LTP、PKC活性和Ng含量的影響 前言 鋁大量蓄積體內可產(chǎn)生毒性作用。國內外許多流行病學調查和研究表明，鋁易致神經(jīng)元損傷，引起智力和認知能力下降等學習和記憶方面的缺欠，且這是一個長期的慢性的神經(jīng)病理過程，涉及到腦發(fā)育的各個階段。 海馬是學習記憶的關鍵腦區(qū)，海馬長時程增強(long-term potentiation，LTP)是NMDA(N-甲基-D-門冬氨酸)受體依賴性突觸傳遞效能的持續(xù)性增強，是公認的腦學習記憶功能在突觸水平的研究模型和神經(jīng)基礎。因此，研究鋁暴露對LTP及與其突觸機制有關的各項生化指標的影響，有助于從突觸和蛋白分子水平闡明鋁損害腦學習記憶功能的作用機制。目前雖然鋁對LTP損害作用的觀察很多，但鋁對LTP損害作用的突觸機制尚未完全闡明。已明確，蛋白激酶C(protein kinase C，PKC)是LTP產(chǎn)生的必需酶，而神經(jīng)顆粒素(Neurogranin，Ng)是一種突觸后腦特異性蛋白質，是PKC的天然作用底物，與LTP的誘導與維持關系密切。同時，母體期是子代腦發(fā)育的一個重要時期，母體期鋁暴露會不會感染子代，是一個關系到子代健康的大問題。因此，本實驗擬采用母體慢性鋁暴露大鼠模型，觀察母體期鋁暴露對子代大鼠海馬LTP誘導和維持、PKC活性及Ng含量的影響，以期從PKC及Ng角度為闡明此發(fā)育階段鋁影響LTP的機制提供一個新視點。 材料與方法 一、實驗材料 1、實驗動物 Wistar大鼠，♀：♂為3：1(體重150-200g)及其所繁殖的子代鼠 2、主要試劑 三氯化鋁(分析純)；抗大鼠Ng單克隆抗體：堿性磷酸酶標記的兔抗山羊二次抗體；PepTag非放射性PKC活性測定試劑盒。 3、主要儀器 大鼠跳臺反應箱；通用電泳儀；凝膠電泳成像系統(tǒng)；低溫冷凍離心機；Spectronic 21型的紫外-可見分光光度計：電生理相關儀器；瓊脂糖凝膠電泳儀。 二、實驗方法 1、分組及動物模型建立 雌性Wistar大鼠45只隨機分為3組，從其與雄性大鼠合籠始至子代斷乳止，在飼料相同條件下，分別飲用蒸餾水、0.2％及0.4％氯化鋁(AlCl_3)溶液。當其子代鼠斷乳(生后21d)后，每窩取出2-3只子代鼠用于實驗，雌雄各半。將飲蒸餾水雌鼠的子代鼠作為對照組(control)，斷乳后繼續(xù)飲用蒸餾水。將飲鋁溶液雌鼠的子代鼠對應分為0.2％和0.4％兩個暴露組(記為0.2％-Al和0.4％-Al組)，斷乳后改飲蒸餾水。每組飲水條件從斷乳至電生理實驗止(時間3-4個月)保持不變，三組動物交替用于實驗。飼養(yǎng)動物的室內溫度18-23℃，相對濕度45-55％。 2、行為學測定 采用跳臺法檢測鋁對學習記憶行為的影響，記錄大鼠第1次跳下平臺的時間(潛伏期)和5 min內受到電擊(即跳下)次數(shù)(錯誤次數(shù))。 3、電生理LTP測定 20％烏拉坦(urethane，6.5ml·kg~(-1)，ip)麻醉后，將動物頭部固定于腦立體定位儀上，在Schaffer側枝部位(坐標：前囟后3.3mm；旁開3.8mm：皮層下3.8mm)插入刺激電極。將記錄玻璃微電極插入海馬CA_1區(qū)部位(坐標：前囟后3.3mm；旁開1.5mm；電極尖端先抵皮層表面，然后逐步推進)行細胞外記錄。找到穩(wěn)定的群體鋒電位(population spike，PS)后，首先記錄30min的每分鐘單脈沖刺激所誘發(fā)的PS。并將所得的30次的PS幅值的平均值作為基線值。然后給予同樣強度及波寬的短串高頻刺激(higll frequency stimuli，HFS)后，觀察每分鐘單脈沖檢驗刺激所誘發(fā)的PS的幅值變化及此變化所持續(xù)的時間。HSF后PS的幅值變化值以相對于基線值的百分數(shù)表示(又稱PS的相對幅值，示PS增強率)。 4、海馬PKC活性的測定 采用瓊脂糖凝膠電泳方法測定海馬PKC的活性。參照PepTag非放射性PKC活性測定試劑盒說明書。 5、Ng含量的測定 采用Western blot方法測定海馬Ng的含量。 6、腦組織及血液中鋁含量測定 采用原子吸收石墨爐法測定腦鋁和血鋁含量。 7、統(tǒng)計學處理 采用SPSS13.0(statistical package for the social science，SPSS)統(tǒng)計分析處理軟件對數(shù)據(jù)進行處理，P＜0.05視為有統(tǒng)計學意義。實驗所得數(shù)據(jù)資料用(?)±S表示。 實驗結果 一、記憶行為學指標 與對照組大鼠第1次跳下平臺的潛伏期(300±0.00秒)相比，0.2％-Al(202.71±81.99秒)和0.4％-Al組(19.67±8.44秒)差異均非常顯著，P＜0.01。兩暴露組5min內錯誤次數(shù)(1.43±0.85次，，2.47±0.99次)與對照組(0.00±0.00次)相比也均存在顯著差異，P＜0.05。兩暴露組之間差異也具有統(tǒng)計學意義，P＜0.01。 二、電生理LTP測試結果 HS后，與對照組PS幅值增強率(143.94±29.93％)相比，0.2％-Al(115.29±14.80％)和0.4％(103.62±13.70％)，差異均非常顯著，P＜0.01。但兩暴露組之間差異不顯著，P＞0.05。 三、海馬PKC活性測定結果(PKC活性單位為pmol／min·mg) 與對照組海馬組織PKC的全細胞(827.60±42.52)、胞膜(340.99±24.50)、胞漿活性(481.32±22.52)及胞膜與胞漿PKC活性比值(0.7114±0.0686)相比，0.2％-Al組(506.41±20.56、155.69±12.63、55.79±25.98、0.4411±0.0623)和0.4％-Al組(494.65±16.81、140.11±4.44、353.44±8.28、0.3966±0.0163)均降低，差異顯著，P＜0.01。但兩暴露組的各項指標差異不顯著，P＞0.05。 四、海馬Ng含量測定結果 與對照組海馬Ng表達的灰度值(62.56±8.74)相比，0.2％-Al組(52.33±4.01)和0.4％-Al組(50.75±5.99)差異顯著，P＜0.01。但兩暴露組之間差異不顯著，P＞0.05。 五、腦組織與血中的鋁含量測定結果 與對照組腦鋁含量(6.21±2.37μg／g)、血鋁含量(33.9±38.74μg／L)相比，0.2％-Al組(15.68±4.48μg/g、47.43±14.38μg/L)和0.4％-Al組(18.79±5.18μg／g、55.56±19.07μg/L)差異均顯著，P＜0.01。但兩暴露組之間差異不顯著，P＞0.05。 討論 母體期是子代腦發(fā)育重要階段，此期的母體鋁暴露對子代腦的智力發(fā)育是否有影響，是一個值得關注的方面。因此，研究鋁及其化合物在母體期的潛在發(fā)育毒性，對鋁導致的兒童智力和認知能力低下性神經(jīng)疾病的早期治療與預防具有重要意義。由實驗結果可見，母體慢性鋁暴露可損害子代海馬LTP的誘導與維持，其損害的程度有隨暴露劑量增加而加重的趨勢，行為學測試的結果也從側面反映了這種關系。腦鋁與血鋁的變化趨勢也基本與之一致。 本實驗結果顯示，母體鋁暴露的子代大鼠的海馬PKC全細胞活性、胞膜、胞漿活性及胞膜與胞漿活性比值，與對照組相比，都分別呈顯著性降低，我們分析認為，鋁通過抑制PKC活性而使LTP產(chǎn)生的必需物質—B-50及NMDA受體的磷酸化調節(jié)發(fā)生障礙，從而損害大鼠LTP及導致其學習記憶能力下降。 本實驗對子代大鼠進行海馬Ng的含量測定結果顯示，與對照組相比，母體鋁暴露的子代大鼠海馬Ng含量下降，有統(tǒng)計學意義。推測Ng含量下降的原因之一可能是樹突棘數(shù)量的減少和細胞缺失，因為有研究表明，鋁負荷過量大鼠海馬CA_1區(qū)神經(jīng)元核固縮和神經(jīng)元減少現(xiàn)象明顯。 總之，對母體實施鋁暴露會影響到子代，且鋁對在LTP機制中起重要作用的PKC和Ng的影響是多方面的，需要進一步的探討。 結論 1、母體期慢性鋁暴露可使子代大鼠第1次跳下平臺的潛伏期縮短，5min內錯誤次數(shù)增加，提示該暴露損害了子代大鼠的記憶能力； 2、母體期慢性鋁暴露可使子代大鼠PS幅值增強率減小，提示該暴露損害了子代大鼠LTP的誘導與維持； 3、母體期慢性鋁損害子代海馬LTP的可能機制之一是鋁造成了其海馬PKC活性和Ng含量的降低。
[Abstract]:Effects of maternal chronic aluminum exposure on LTP, PKC activity and Ng content in hippocampus of offspring rats
Preface
Many epidemiological investigations and studies at home and abroad have shown that aluminum is vulnerable to neuronal damage, causing a lack of learning and memory, such as intellectual and cognitive decline, and this is a chronic, chronic neuropathological process, involving various stages of brain development.
Hippocampus is the key brain area for learning and memory. Long-term potentiation (LTP) is a continuous enhancement of NMDA (N- methy aspartic acid) receptor dependent synaptic transmission efficiency. It is a recognized model of brain learning and memory function at the synaptic level and the basis of the apex. Therefore, the study of aluminum exposure to LTP and its synaptic mechanism The effects of various biochemical indexes are helpful to elucidate the mechanism of aluminum damage to brain learning and memory function from the synapse and protein molecular level. Although there are many observations on the damage effect of aluminum to LTP, the synaptic mechanism of aluminum damage to LTP has not been fully elucidated. It is clear that the egg white kinase C (protein kinase C, PKC) is a necessity for LTP production. Neurogranin (Ng) is a specific protein of the postsynaptic brain, which is a natural protein of the postsynaptic brain. It is a natural substrate for PKC. It is closely related to the induction and maintenance of LTP. At the same time, the parent phase is an important period for the development of the progeny of the offspring. The model of maternal chronic aluminum exposure was used to observe the effect of aluminum exposure on LTP induction and maintenance, PKC activity and the content of Ng in the hippocampus of the parent rat, in order to provide a new view from the angle of PKC and Ng to elucidate the mechanism of aluminum affecting LTP at this stage.
Materials and methods
First, experimental materials
1, experimental animals
Wistar rats were: 3:1 (body weight 150-200g) and their offspring offspring.
2, the main reagent
Aluminum chloride (analytical purity); anti rat Ng monoclonal antibody: alkaline phosphatase labeled Rabbit anti goat two antibody; PepTag non radioactive PKC activity assay kit.
3, the main instrument
Rat platform reaction box; general electrophoretic apparatus; gel electrophoresis imaging system; cryogenic centrifuge; Spectronic 21 ultraviolet visible spectrophotometer: electrophysiological related instrument; agarose gel electrophoresis apparatus.
Two, experimental method
1, group and animal model establishment
45 female Wistar rats were randomly divided into 3 groups, from the cages of the male rats to the offspring of the offspring. Under the same feed conditions, drinking distilled water, 0.2% and 0.4% aluminum chloride (AlCl_3) solution respectively. When their offspring were weaned (after birth 21d), 2-3 offspring were taken out of each nest. As a control group (control), drinking distilled water was continued after weaning. The offspring of female rats were divided into 0.2% and 0.4% exposed groups (group 0.2%-Al and 0.4%-Al), and distilled water was changed after weaning. Each group of drinking water remained unchanged from weaning to electrophysiological experiment (3-4 months), and three groups were used alternately for experiment. The indoor temperature of raising animals is 18-23 degrees, and the relative humidity is 45-55%.
2, behavioural determination
The effect of aluminum on learning and memory behavior was detected by platform method. The time (incubation period) and the number of times (the number of errors) were recorded in the time (incubation period) of the first jumping platform and the 5 min in the rats.
3, electrophysiological LTP determination
After 20% uran (urethane, 6.5ml. Kg~ (-1), IP), the head of the animal was fixed on the brain stereotaxic. The stimulation electrode was inserted into the Schaffer lateral branch (coordinates: 3.3mm in the anterior fontanelle, 3.8mm: subcortical 3.8mm), and the glass microelectrodes were inserted into the hippocampus CA_1 region (coordinates: the fontanelle, 3.3mm; the side opening 1.5mm; the tip tip). When the stable group front potential (population spike, PS) was found, the PS. was first recorded by the single pulse of 30min and the mean value of the 30 PS amplitude was taken as the baseline value. Then the short series of high frequency stimulation (higll frequenc) with the same intensity and wave width (higll frequenc) was given. After y stimuli, HFS), the amplitude changes of the PS induced by the monopulse test per minute and the duration of this change are observed after.HSF, and the amplitude of PS is expressed as a percentage relative to the baseline value (also known as the relative amplitude of the PS, showing the PS enhancement rate).
4, determination of the activity of PKC in the hippocampus
The activity of hippocampal PKC was determined by agarose gel electrophoresis. Reference to PepTag non radioactive PKC activity assay kit was provided.
5, determination of Ng content
The Western blot method was used to determine the content of Ng in the hippocampus.
6, determination of aluminum content in brain tissue and blood
Atomic absorption graphite furnace method was used to determine the content of aluminum and aluminum in brain.
7, statistical treatment
The data are processed with SPSS13.0 (statistical package for the social science, SPSS) statistical analysis and analysis processing software. P < 0.05 is statistically significant. The data obtained from the experiment are expressed in (?) + S.
experimental result
First, the index of memory behavior
Compared with the incubation period of first times (300 + 0 seconds), 0.2%-Al (202.71 + 81.99 seconds) and 0.4%-Al group (19.67 + 8.44 seconds) were significantly different from the control group. The number of errors in 5min in the P < 0.01. two exposure group (1.43 + 0.85, 2.47 + 0.99) was also significantly different from the control group (0 + 0), P < 0.05. exposure group. The difference was also statistically significant, P < 0.01.
Two, electrophysiological LTP test results
After HS, compared with the contrast group PS amplitude enhancement rate (143.94 + 29.93%), 0.2%-Al (115.29 + 14.80%) and 0.4% (103.62 + 13.70%), the difference was very significant, P < 0.01., but there was no significant difference between the two exposed groups, P > 0.05.
Three, the results of hippocampal PKC activity assay (PKC activity unit was pmol / min mg).
The whole cell (827.60 + 42.52) of PKC in the hippocampus of the control group, the membrane (340.99 + 24.50), cytoplasm activity (481.32 + 22.52) and the ratio of cytoplasmic PKC activity (0.7114 + 0.0686), 0.2%-Al group (506.41 + 20.56155.69 + 12.63,55.79 + 25.98,0.4411 + 0.0623) and 0.4%-Al group (494.65 + 16.81140.11 + 4.44353.44 + 8.28,0.3966 + 0.0163) The difference was significant, P < 0.01., but the difference between the two exposure groups was not significant, P > 0.05.
Four, the results of the determination of Ng content in the hippocampus
Compared with the gray value of Ng expression in the hippocampus of the control group (62.56 + 8.74), the difference between the 0.2%-Al group (52.33 + 4.01) and the 0.4%-Al group (50.75 + 5.99) was significant, P < 0.01., but there was no significant difference between the two exposed groups, P > 0.05.
Five, determination of aluminum content in brain tissue and blood
Compared with the control group, the content of Al (6.21 + 2.37 g / g) and the content of blood aluminum (33.9 + 38.74 mu g / L), 0.2%-Al group (15.68 + 4.48 g/g, 47.43 + 14.38 mu g/L) and 0.4%-Al group (18.79 + 5.18 mu / g, 55.56 + 19.07 mu g/L) were all significant differences.
discuss
The maternal stage is an important stage of the subgeneration brain development, and the maternal aluminum exposure in this period is an important aspect of the intellectual development of the offspring brain. Therefore, the study of the potential developmental toxicity of aluminum and its compounds in the parent phase is important for the early treatment and prevention of mental and cognitive impairment of the aluminum induced children. The experimental results showed that the maternal chronic aluminum exposure could damage the induction and maintenance of the hippocampal LTP in the offspring, and the degree of damage increased with the increase of exposure dose. The results of the behavioral test also reflected the relationship. The trend of the change of brain aluminum and blood aluminum was also basically consistent.
The results showed that the PKC whole cell activity, the cell membrane, the cytoplasm activity and the ratio of the cytoplasm and cytoplasm activity of the offspring of the maternal aluminum exposed rats were significantly lower than those of the control group. In our analysis, we believe that the aluminum by inhibiting the activity of PKC makes the phosphorylation of the necessary substance produced by LTP produced by LTP and the phosphorylation of the NMDA receptor to occur. It can damage LTP and decrease learning and memory ability in rats.
In this experiment, the content determination of hippocampal Ng in the offspring of the offspring showed that compared with the control group, the content of Ng in the hippocampus of the offspring of the maternal aluminum exposed rats decreased, which was statistically significant. One of the reasons for the decrease of Ng content may be the decrease of the number of dendritic spines and the loss of cells. The phenomenon of pyknosis and neuron reduction in the nucleus was obvious.
In conclusion, the exposure to maternal aluminum will affect the offspring, and the effects of aluminum on PKC and Ng, which play an important role in the LTP mechanism, are multifaceted and need further exploration.
conclusion
1, chronic aluminum exposure in the mother stage could shorten the incubation period of the first descending platform of the offspring and increase the number of errors in 5min, suggesting that the exposure damage the memory ability of the offspring of the offspring.
2, maternal exposure to chronic aluminum exposure reduced the amplitude of PS in offspring rats, suggesting that the exposure impaired the induction and maintenance of LTP in offspring rats.
3, one of the possible mechanisms of maternal chronic aluminum damage in offspring hippocampus LTP is that aluminum causes the decrease of PKC activity and Ng content in hippocampus.
【學位授予單位】：中國醫(yī)科大學
【學位級別】：碩士
【學位授予年份】：2007
【分類號】：R363

【相似文獻】

相關期刊論文 前10條

1 陶哠嫣;唐小曼;謝玉波;;異丙酚對新生大鼠海馬突觸后致密物-95和突觸素表達的影響[J];廣東醫(yī)學;2011年13期

2 唐倩;夏茵茵;程淑群;涂白杰;;苯并芘對大鼠海馬組織基因表達影響[J];中國公共衛(wèi)生;2011年08期

3 王哲;王守巖;王德山;馬賢德;高原;趙金茹;關洪全;;眼針對急性腦缺血再灌注損傷大鼠海馬組織BDNF表達影響[J];針灸臨床雜志;2011年07期

4 肖娟娟;王秋桂;張敏海;;慢性復合應激對成年海馬FGF-2的表達及神經(jīng)發(fā)生的影響[J];中國組織化學與細胞化學雜志;2011年03期

5 宗志紅;王彪;;慢性鋁暴露對雄性大鼠海馬組織中TLR2蛋白及其mRNA表達的影響[J];環(huán)境與健康雜志;2011年03期

6 唐倩;夏茵茵;程淑群;涂白杰;;苯并芘對大鼠記憶及谷氨酸鹽受體基因表達影響[J];中國公共衛(wèi)生;2011年07期

7 李肖云;蘭希發(fā);;粒細胞集落刺激因子對血管性癡呆大鼠海馬神經(jīng)細胞凋亡的影響[J];中國組織工程研究與臨床康復;2011年27期

8 李潺;胡江;聞大翔;杭燕南;;丙泊酚對糖尿病大鼠海馬組織蛋白質表達影響的蛋白組學研究[J];上海交通大學學報(醫(yī)學版);2011年06期

9 張冠楠;鄂建羽;殷曉莉;;針刺督脈穴對血管性癡呆模型大鼠行為及細胞凋亡影響的實驗研究[J];遼寧中醫(yī)雜志;2011年08期

10 張泓波;高維娟;錢濤;唐敬龍;李君;;補陽還五湯提高血管性癡呆大鼠海馬CREB、C/EBP的DNA結合活性[J];中國藥理學通報;2011年08期

相關會議論文 前10條

1 陳瀑;沈愛國;甘勝偉;袁華;王小華;胡繼明;;阿爾茲海默氏癥大鼠海馬組織的拉曼光譜表征[A];第十四屆全國光散射學術會議論文摘要集[C];2007年

2 婁鵬程;焦穎;林忠東;葉秀云;王海萍;李光乾;;Z-ATAD-FMK對癲癇持續(xù)狀態(tài)后大鼠海馬Caspase-12、3表達和神經(jīng)元凋亡的影響[A];第六屆江浙滬兒科學術會議暨兒科學基礎與臨床研究進展學術班論文匯編[C];2009年

3 聶坤;于建春;成海燕;潘建明;韓景獻;;SAMP10鼠海馬組織AKT表達和活化的增齡變化[A];第八屆全國中西醫(yī)結合實驗醫(yī)學研討會論文匯編[C];2006年

4 孔立紅;徐珉;周華;孫國杰;;電針對腦缺血再灌注大鼠海馬組織STAT3表達及核轉位的影響[A];第九屆全國針刺麻醉針刺鎮(zhèn)痛及針刺調整效應學術研討會論文集[C];2007年

5 張雪娜;岳云;劉揚;徐志鵬;楊樹廣;劉少君;;異丙酚麻醉影響大鼠海馬可溶蛋白的比較蛋白質組學研究[A];2008年中華醫(yī)學會全國麻醉學術年會論文匯編[C];2008年

6 鐘樹志;李喬;馬世平;;基于抗炎作用的當歸芍藥散抗AD的實驗研究[A];第五屆全國中醫(yī)藥免疫學術研討會——暨環(huán)境·免疫與腫瘤防治綜合交叉會議論文匯編[C];2009年

7 孔立紅;孫國杰;;針刺對腦缺血再灌注大鼠海馬組織NF-κB表達及含量的影響[A];中國針灸學會2005年學術年會論文匯編[C];2005年

8 王濤;文亮;;全腦缺血/再灌注海馬ICE的表達及其在神經(jīng)元損傷中的作用[A];第十一次全國急診醫(yī)學學術會議暨中華醫(yī)學會急診醫(yī)學分會成立二十周年慶典論文匯編[C];2006年

9 王晟;鄒湘輝;黃慶軍;;母愛剝奪對小鼠學習記憶和海馬形態(tài)結構的影響[A];中華醫(yī)學會精神病學分會第七屆學術年會論文摘要集[C];2006年

10 陳耀光;施靜;;電針治療大鼠腦缺血再灌注損傷中對海馬Anne×in A1調節(jié)作用[A];節(jié)能環(huán)保 和諧發(fā)展——2007中國科協(xié)年會論文集（二）[C];2007年

相關重要報紙文章 前10條

1 龔正;防止記憶衰退并不難[N];醫(yī)藥養(yǎng)生保健報;2009年

2 韋辰;6種方法防記憶力減退[N];大眾科技報;2005年

3 錢耀斌;增強記憶力的六大法則[N];大眾衛(wèi)生報;2007年

4 常碩;防止記憶力減退六招[N];醫(yī)藥養(yǎng)生保健報;2005年

5 黃文;五種方法防止記憶力衰退[N];中國中醫(yī)藥報;2006年

6 匡遠深;興奮性突觸功能增強是癲癇反復發(fā)作根源[N];健康報;2008年

7 記者 匡遠深;癲癇放射外科治療動物模型建立[N];健康報;2008年

8 王振嶺;高碘危害人體器官[N];科技日報;2001年

9 謝寧;黑龍江中醫(yī)藥大學確定補腎健脾、化痰開竅法治療AD原理[N];中國醫(yī)藥報;2005年

10 中國工程院院士 肖培根;中藥基因組學 為中醫(yī)藥現(xiàn)代化提速[N];醫(yī)藥導報;2002年

相關博士學位論文 前10條

1 胡永波;抑郁模型大鼠海馬突觸蛋白質組學初步研究[D];重慶醫(yī)科大學;2011年

2 姜聲揚;X射線輻照后對中樞海馬組織損傷作用研究[D];蘇州大學;2012年

3 楊瑩;海馬依賴性情節(jié)記憶調控的突觸和神經(jīng)環(huán)路機制研究[D];華中科技大學;2012年

4 崔博;噪聲暴露對認知功能的影響及其海馬機制研究[D];中國人民解放軍軍事醫(yī)學科學院;2010年

5 孟培燕;電針對血管性癡呆大鼠學習記憶相關信號通路影響的研究[D];湖北中醫(yī)學院;2007年

6 劉亞君;缺血預處理抗大鼠海馬神經(jīng)元缺血再灌注損傷的線粒體機制[D];山東大學;2007年

7 陳亮;參與腦缺血損傷和保護機制的蛋白靶點篩查[D];第一軍醫(yī)大學;2007年

8 李洪;肝郁證模型大鼠海馬差異基因表達譜的研究[D];南方醫(yī)科大學;2009年

9 程淑群;苯并[a]芘對大鼠學習記憶的影響及其機制研究[D];重慶醫(yī)科大學;2009年

10 張翔南;LPS腹腔注射誘發(fā)大鼠腦內炎癥致皮層與海馬病理改變及相關機制研究[D];浙江大學;2010年

相關碩士學位論文 前10條

1 趙卓;母體期慢性鋁暴露對子代大鼠海馬LTP、PKC活性和Ng含量的影響[D];中國醫(yī)科大學;2007年

2 沈瑞樂;丁基苯酞對慢性腦缺血老齡大鼠海馬區(qū)Chat的影響[D];鄭州大學;2007年

3 馬俊驥;老年大鼠的空間學習記憶能力下降與海馬背側膽固醇含量增加有關[D];河北醫(yī)科大學;2006年

4 張沙駱;低氧訓練對大鼠海馬組織細胞凋亡的影響[D];湖南師范大學;2007年

5 鄭永麗;海馬組織發(fā)育過程中基因調控網(wǎng)絡構建的生物動力學模型研究[D];第三軍醫(yī)大學;2007年

6 趙久紅;缺氧對新生大鼠海馬神經(jīng)干細胞增殖分化的影響[D];中國醫(yī)科大學;2009年

7 唐源遠;胰島素誘導低血糖對新生大鼠海馬神經(jīng)干細胞增殖和分化的影響[D];中國醫(yī)科大學;2009年

8 陳志斌;氯胺酮對SD幼鼠海馬神經(jīng)元突觸素、GAP-43的影響[D];第三軍醫(yī)大學;2005年

9 王U

本文編號：2110077