中华行为医学与脑科学杂志
中華行為醫學與腦科學雜誌
중화행위의학여뇌과학잡지
CHINESE JOURNAL OF BEHAVIORAL MEDICINE AND BRAIN SCIENCE
2012年
12期
1060-1063
,共4页
程丽%景玮%王改弟%郭亮%祁金顺
程麗%景瑋%王改弟%郭亮%祁金順
정려%경위%왕개제%곽량%기금순
长时程压抑%β淀粉样蛋白%海马%阿尔茨海默病
長時程壓抑%β澱粉樣蛋白%海馬%阿爾茨海默病
장시정압억%β정분양단백%해마%아이자해묵병
Long-term depression%Amyloid β protein%Hippocampus%Alzheimer's disease
目的 探讨在体诱导大鼠海马CA1区长时程压抑(LTD)的诱导条件以及淀粉样β蛋臼(Aβ)对其影响.方法 给予大鼠海马CA1区Schaffer侧枝测试刺激,以诱发在体场兴奋性突触后电位(fEPSPs)；进一步比较不同的低频刺激(LFS)对LTD诱导的作用,并观察侧脑室注射不同剂量的Aβ25-35对LTD的影响.结果 双脉冲刺激(PPS)不能有效地诱导出大鼠海马CA1区的LTD;长时间给予频率为1,5和10 Hz的LFS后,fEPSPs的幅度迅速下降,明显(P＜0.05)低于LFS前水平；LFS后120 min,1 Hz 900个脉冲的LFS诱导的LTD为(63.7±3.8)％,比1Hz 600个脉冲组的(75.1±3.2)％更为明显(P＜0.05)；而同时间点刺激脉冲数相同(900个)、刺激频率不同(1,5和10 Hz)的三组LFS诱导的LTD程度相似(P＞0.05),分别为(63.7±3.8)％,(61.2±3.6)％和(59.8±3.9)％；脑室注射较低剂量(12.5 nmol)的Aβ25-35后,LFS诱导的LTD为(63.2±3.8)％,明显低于对照组的(73.9±3.0)％(P＜0.05),较大剂量(25nmol) Aβ25-35则使LTD现象更加明显,LFS后120 min为(46.8±3.9)％,低于12.5 nmol Aβ25-35组(P＜0.05)和对照组(P＜0.01).结论 长时间的LFS能有效诱发在体大鼠海马CA1区LTD,这为记录在体海马LTD和从事突触可塑性研究提供了重要的实验参数；脑室注射Aβ25-35不影响海马CA1区基础突触传递,但能增强LTD,提示阿尔茨海默病患者早期出现的学习记忆功能障碍可能与Aβ干扰脑内突触可塑性有关.
目的 探討在體誘導大鼠海馬CA1區長時程壓抑(LTD)的誘導條件以及澱粉樣β蛋臼(Aβ)對其影響.方法 給予大鼠海馬CA1區Schaffer側枝測試刺激,以誘髮在體場興奮性突觸後電位(fEPSPs)；進一步比較不同的低頻刺激(LFS)對LTD誘導的作用,併觀察側腦室註射不同劑量的Aβ25-35對LTD的影響.結果 雙脈遲刺激(PPS)不能有效地誘導齣大鼠海馬CA1區的LTD;長時間給予頻率為1,5和10 Hz的LFS後,fEPSPs的幅度迅速下降,明顯(P＜0.05)低于LFS前水平；LFS後120 min,1 Hz 900箇脈遲的LFS誘導的LTD為(63.7±3.8)％,比1Hz 600箇脈遲組的(75.1±3.2)％更為明顯(P＜0.05)；而同時間點刺激脈遲數相同(900箇)、刺激頻率不同(1,5和10 Hz)的三組LFS誘導的LTD程度相似(P＞0.05),分彆為(63.7±3.8)％,(61.2±3.6)％和(59.8±3.9)％；腦室註射較低劑量(12.5 nmol)的Aβ25-35後,LFS誘導的LTD為(63.2±3.8)％,明顯低于對照組的(73.9±3.0)％(P＜0.05),較大劑量(25nmol) Aβ25-35則使LTD現象更加明顯,LFS後120 min為(46.8±3.9)％,低于12.5 nmol Aβ25-35組(P＜0.05)和對照組(P＜0.01).結論 長時間的LFS能有效誘髮在體大鼠海馬CA1區LTD,這為記錄在體海馬LTD和從事突觸可塑性研究提供瞭重要的實驗參數；腦室註射Aβ25-35不影響海馬CA1區基礎突觸傳遞,但能增彊LTD,提示阿爾茨海默病患者早期齣現的學習記憶功能障礙可能與Aβ榦擾腦內突觸可塑性有關.
목적 탐토재체유도대서해마CA1구장시정압억(LTD)적유도조건이급정분양β단구(Aβ)대기영향.방법 급여대서해마CA1구Schaffer측지측시자격,이유발재체장흥강성돌촉후전위(fEPSPs)；진일보비교불동적저빈자격(LFS)대LTD유도적작용,병관찰측뇌실주사불동제량적Aβ25-35대LTD적영향.결과 쌍맥충자격(PPS)불능유효지유도출대서해마CA1구적LTD;장시간급여빈솔위1,5화10 Hz적LFS후,fEPSPs적폭도신속하강,명현(P＜0.05)저우LFS전수평；LFS후120 min,1 Hz 900개맥충적LFS유도적LTD위(63.7±3.8)％,비1Hz 600개맥충조적(75.1±3.2)％경위명현(P＜0.05)；이동시간점자격맥충수상동(900개)、자격빈솔불동(1,5화10 Hz)적삼조LFS유도적LTD정도상사(P＞0.05),분별위(63.7±3.8)％,(61.2±3.6)％화(59.8±3.9)％；뇌실주사교저제량(12.5 nmol)적Aβ25-35후,LFS유도적LTD위(63.2±3.8)％,명현저우대조조적(73.9±3.0)％(P＜0.05),교대제량(25nmol) Aβ25-35칙사LTD현상경가명현,LFS후120 min위(46.8±3.9)％,저우12.5 nmol Aβ25-35조(P＜0.05)화대조조(P＜0.01).결론 장시간적LFS능유효유발재체대서해마CA1구LTD,저위기록재체해마LTD화종사돌촉가소성연구제공료중요적실험삼수；뇌실주사Aβ25-35불영향해마CA1구기출돌촉전체,단능증강LTD,제시아이자해묵병환자조기출현적학습기억공능장애가능여Aβ간우뇌내돌촉가소성유관.
Objective To investigate the exact protocol eliciting the hippocampal CA1 long-term depression (LTD) of rats in vivo and the effect of amyloid β-protein (Aβ) on the LTD.Method By applying test stimulation to Schaffer collateral in hippocampal CA1 region in rats,recorded the in vivo field excitatory postsynaptic potentials (fEPSPs) ;further,observed the induction of LTD with different low frequency stimulation (LFS) and investigated the effect of Aβ25-35 on the LTD.Results Prolonged LFS (1,5 and 10 Hz) but not paired-pulse stimulus (PPS) effectively elicited the LTD in the hippocampal CA1 region,with significantly decreased amplitude of fEPSPs after LFS ; 1 Hz 900 pulses group induced a stronger LTD,being (63.7 ± 3.8) ％ at 120 min post-LFS,lower (P ＜ 0.05) than (75.1 ± 3.2) ％ in 600 pulses group ; different frequencies (1,5 and 10 Hz) of LFS with same pulses induced similar degree of LTD,the amplitude of fEPSPs were (63.7 ± 3.8) ％,(61.2 ± 3.6) ％ and (59.8 ± 3.9) ％ respectively,without significant differences between any two groups (P ＞ 0.05) ; after applying 12.5 nmol and 25 nmol Aβ25-35,the amplitude of fEPSPs decreased to (63.2 ± 3.8) ％ and (46.8 ± 3.9) ％,respectively,and lower and than that in control ((73.9 ± 3.0) ％,P ＜ 0.05).Conclusion Prolonged LFS effectively induced in vivo hippocampal LTD of rats,which provides an important electrophysiological protocol for the study of synaptic plasticity; Aβ25-35 injection dont affect the baseline synaptic transmission,but dose-dependently enhance the in vivo hippocampal LTD of rats,indicating that Aβ-induced LTD facilitation may be involved the early impairment of learning and memory in Alzheimer's disease.
