據(jù)9月18日的《科學(xué)》雜志報道說,，對患有Alzheimer氏病的小鼠的腦子進(jìn)行掃描發(fā)現(xiàn)了一類“活動亢進(jìn)的”神經(jīng)元,，它們與該疾病的癥狀有關(guān)聯(lián),。這些活動亢進(jìn)的神經(jīng)元最密集地集中在病變腦組織中所發(fā)現(xiàn)的淀粉樣斑塊沉積處的附近,，而它們的存在可能是癲癇樣發(fā)作增加的基礎(chǔ),。
Marc Aurel Busche及其同僚應(yīng)用雙光子Ca2+ 成像來對受到Alzheimer氏癥影響的小鼠腦中正在發(fā)生的活動進(jìn)行檢測,。他們發(fā)現(xiàn)腦組織中有整整一半的神經(jīng)元的沖動發(fā)放速度是在其正常范圍之外的——即沖動發(fā)放或者太快或者太慢。
研究人員提示,，這種亢進(jìn)是因為突觸抑制受到損害引起的,，而非因為激發(fā)正常神經(jīng)元沖動發(fā)放的Ca2+釋放的波動所引起的。他們還說,，這種在淀粉樣斑塊附近的快速發(fā)放的活動亢進(jìn)神經(jīng)元是以一種互為關(guān)聯(lián)的方式發(fā)放沖動的,，從而增加了癲癇發(fā)生的危險。這種新的Alzheimer病的小鼠模型可以為將來治療這種疾病提供主意,。（生物谷Bioon.com）
生物谷推薦原始出處：
Science 19 September 2008: Vol. 321. no. 5896, pp. 1686 - 1689 DOI: 10.1126/science.1162844
Clusters of Hyperactive Neurons Near Amyloid Plaques in a Mouse Model of Alzheimer's Disease
Marc Aurel Busche,1,4 Gerhard Eichhoff,1,4 Helmuth Adelsberger,1,4 Dorothee Abramowski,2 Karl-Heinz Wiederhold,2 Christian Haass,3,4 Matthias Staufenbiel,2 Arthur Konnerth,1,4* Olga Garaschuk1,4
The neurodegeneration observed in Alzheimer's disease has been associated with synaptic dismantling and progressive decrease in neuronal activity. We tested this hypothesis in vivo by using two-photon Ca2+ imaging in amouse model of Alzheimer's disease. Although a decrease in neuronal activity was seen in 29% of layer 2/3 corticalneurons, 21% of neurons displayed an unexpected increase in the frequency of spontaneous Ca2+ transients. These"hyperactive" neurons were found exclusively near the plaques of amyloid β–depositing mice. The hyperactivityappeared to be due to a relative decrease in synaptic inhibition. Thus, we suggest that a redistribution of synaptic drive between silent and hyperactive neurons, rather than an overall decrease in synaptic activity, provides amechanism for the disturbed cortical function in Alzheimer's disease.
