华东师范大学学报(自然科学版)
華東師範大學學報(自然科學版)
화동사범대학학보(자연과학판)
JOURNAL OF EAST CHINA NORMAL UNIVERSITY(NATURAL SCIENCE)
2010年
2期
111-118
,共8页
安述明%曾庆文%徐浩%刘汝清%曹晓华
安述明%曾慶文%徐浩%劉汝清%曹曉華
안술명%증경문%서호%류여청%조효화
钙/钙调蛋白依赖性蛋白激酶Ⅱ%疲劳转棒实验%Morris水迷宫实验%LTD%空间再学习
鈣/鈣調蛋白依賴性蛋白激酶Ⅱ%疲勞轉棒實驗%Morris水迷宮實驗%LTD%空間再學習
개/개조단백의뢰성단백격매Ⅱ%피로전봉실험%Morris수미궁실험%LTD%공간재학습
CaMKII%rotarod test%Morris water maze%LTD%spatial reversal learning
将3月龄实验小鼠分为αCaMKII-F89G转基因组和同窝野生对照组,进行疲劳转棒实验和Morris水迷宫实验测试.结果显示,转基因组小鼠的体力和运动协调能力与对照组相比无显著的差异;在Morris水迷宫实验的可视平台测试中,转基因鼠的视觉和求生的动机表现正常;在定位航行训练和第一次空间探索测试中,两组鼠在训练时逃避潜伏期及测试中在目标象限探索时间无统计学差异;但是在反向定位空间学习阶段,转基因组在第二、三天逃避潜伏期和距离明显长于同窝对照组(P <0.05).由此认为,αCaMKII在前脑过量表达对小鼠的灵活性学习有损伤作用,推测这种损伤有可能由前脑LTD的缺陷造成的.
將3月齡實驗小鼠分為αCaMKII-F89G轉基因組和同窩野生對照組,進行疲勞轉棒實驗和Morris水迷宮實驗測試.結果顯示,轉基因組小鼠的體力和運動協調能力與對照組相比無顯著的差異;在Morris水迷宮實驗的可視平檯測試中,轉基因鼠的視覺和求生的動機錶現正常;在定位航行訓練和第一次空間探索測試中,兩組鼠在訓練時逃避潛伏期及測試中在目標象限探索時間無統計學差異;但是在反嚮定位空間學習階段,轉基因組在第二、三天逃避潛伏期和距離明顯長于同窩對照組(P <0.05).由此認為,αCaMKII在前腦過量錶達對小鼠的靈活性學習有損傷作用,推測這種損傷有可能由前腦LTD的缺陷造成的.
장3월령실험소서분위αCaMKII-F89G전기인조화동와야생대조조,진행피로전봉실험화Morris수미궁실험측시.결과현시,전기인조소서적체력화운동협조능력여대조조상비무현저적차이;재Morris수미궁실험적가시평태측시중,전기인서적시각화구생적동궤표현정상;재정위항행훈련화제일차공간탐색측시중,량조서재훈련시도피잠복기급측시중재목표상한탐색시간무통계학차이;단시재반향정위공간학습계단,전기인조재제이、삼천도피잠복기화거리명현장우동와대조조(P <0.05).유차인위,αCaMKII재전뇌과량표체대소서적령활성학습유손상작용,추측저충손상유가능유전뇌LTD적결함조성적.
The αCaMKII-F89G transgenic mice and their littermate controls were subjected to the rotarod test and Morris water maze test.There was no significant difference in motor coordination and ability between these two groups in the rotarod test.In the visible platform test, transgenic mice showed the normal perception, motivation and motor ability.In addition, transgenic mice performed normally in learning and memory in both place navigation training and the 1st spatial probe test.However, compared with wild type mice, transgenic mice spent significantly more time and swam longer distance to reach hidden platform in the 2nd and 3rd day of spatial reversal learning.These results indicate that αCaMKII overexpression in the forebrain can impair spatial reversal learning.The mechanism of the performance deficit may be relevant to disrupted or abolished LTD in the forebrain.