生物谷報(bào)道:都說(shuō)熟能生巧,至少我們的父輩一再的告訴我們,,通過(guò)不斷的練習(xí)積累個(gè)人經(jīng)驗(yàn)就能在某一方面出眾。但是讓神經(jīng)生物學(xué)家困惑的是,,數(shù)據(jù)表明單個(gè)突觸,,或神經(jīng)元之間的聯(lián)系雖然增多了,而重復(fù)刺激卻會(huì)在減弱神經(jīng)突觸的作用,。
近期來(lái)自卡耐基-梅隆大學(xué)(Carnegie Mellon University)神經(jīng)認(rèn)知中心(The Center for the Neural Basis of Cognition ,,CNBC),德國(guó)馬克斯-普朗克醫(yī)學(xué)研究所(Max Planck Institute for Medical Research)的研究人員發(fā)現(xiàn)了一種新機(jī)制,,解釋了這一似是而非的問(wèn)題,。這一研究成果公布在昨天出版(2008年1月4日)的Science雜志上。
領(lǐng)導(dǎo)這一研究的是卡耐基-梅隆大學(xué)的Alison Barth博士,。
這一機(jī)制進(jìn)一步解釋了在應(yīng)答新體驗(yàn)的時(shí)候大腦神經(jīng)突觸如何加強(qiáng)的,,之前卡耐基-梅隆大學(xué)的研究人員發(fā)現(xiàn)在突觸可塑性(或改變)與學(xué)習(xí)記憶之間存在關(guān)聯(lián),但是有關(guān)通過(guò)不斷的聯(lián)系進(jìn)行長(zhǎng)時(shí)間學(xué)習(xí)的認(rèn)知活動(dòng)的機(jī)制,,至今了解的很少,。
現(xiàn)在研究人員發(fā)現(xiàn)N-甲基-D-天門(mén)冬氨酸(NMDA,生物谷注)受體在啟動(dòng)突觸可塑性方面的重要作用,,NMDA受體在中樞神經(jīng)系統(tǒng)信號(hào)傳遞以及神經(jīng)系統(tǒng)的可塑性方面具有重要的作用,,2005年科學(xué)家們?cè)贜ature雜志上報(bào)道了NMDA受體激動(dòng)劑結(jié)合部位的晶體結(jié)構(gòu) (crystal structures) ,,證明了四聚體(tetrameric)的NMDA受體是有異性雙聚體(heterodimer)的NR1–NR2A構(gòu)成。
Barth和她的同事發(fā)現(xiàn)NMDA受體在學(xué)習(xí)的最初階段開(kāi)始之后能進(jìn)行一種吉柯與海德(Jekyll-and-Hyde,,又稱為化身博士,,指一個(gè)人格分裂的博士,白天正直善良,,晚上作惡多端,,生物谷注)式的轉(zhuǎn)變。除了幫助突觸變得更加強(qiáng)大之外,,它們實(shí)際上也會(huì)消弱突觸的作用,,破壞進(jìn)一步的學(xué)習(xí)認(rèn)知。Barth認(rèn)為,,科學(xué)家們研究發(fā)現(xiàn)在最初的學(xué)習(xí)或練習(xí)經(jīng)歷之后,,這種受體功能的改變,以及對(duì)于突觸的影響也許意味著學(xué)習(xí)會(huì)停止,,而且持續(xù)的刺激神經(jīng)的過(guò)程也許會(huì)退化——然而實(shí)際經(jīng)驗(yàn)并不是這樣,。
Barth表示,“我們直覺(jué)上認(rèn)為,,我們練習(xí)得越多,,在這一方面我們就會(huì)作得更好,因此在NMDA受體轉(zhuǎn)換幫助突觸加強(qiáng)得這一功能之后,,應(yīng)該發(fā)生了其它事情,。”
因此研究人員將目光轉(zhuǎn)移到了大腦皮層(cortex)——一個(gè)大腦的區(qū)域,負(fù)責(zé)額外訓(xùn)練或體驗(yàn)?zāi)茉黾訉W(xué)習(xí)的一個(gè)較慢形式,,Barth等人注意到這個(gè)大腦的區(qū)域利用了與短時(shí)程的,,情景記憶(episodic memory,生物谷注)的其它形式存在差異十分大的分子機(jī)制,,情景記憶即指在海馬組織種出現(xiàn)的記憶,。
生物谷推薦原始出處:
Science 4 January 2008:
Vol. 319. no. 5859, pp. 101 - 104
DOI: 10.1126/science.1143808
Ongoing in Vivo Experience Triggers Synaptic Metaplasticity in the Neocortex
Roger L. Clem,1 Tansu Celikel,2* Alison L. Barth1
In vivo experience can occlude subsequent induction of long-term potentiation and enhance long-term depression of synaptic responses. Although a reduced capacity for synaptic strengthening may function to prevent excessive excitation, such an effect paradoxically implies that continued experience or training should not improve and may even degrade neural representations. In mice, we examined the effect of ongoing whisker stimulation on synaptic strengthening at layer 4-2/3 synapses in the barrel cortex. Although N-methyl-D-aspartate receptors were required to initiate strengthening, they subsequently suppressed further potentiation at these synapses in vitro and in vivo. Despite this transition, synaptic strengthening continued with additional sensory activity but instead required the activation of metabotropic glutamate receptors, suggesting a mechanism by which continued experience can result in increasing synaptic strength over time.
1 Department of Biological Sciences and Center for the Neural Basis of Cognition, Carnegie Mellon University, Pittsburgh, PA 15213, USA.
2 Department of Cell Physiology, Max Planck Institute for Medical Research, Jahnstrasse 29, 69120 Heidelberg, Germany.
* Present address: Laboratory of Neural Circuits and Plasticity, University of Southern California, 3641 Watt Way, HNB 501, Los Angeles, CA 90089-2520, USA.
To whom correspondence should be addressed. E-mail: [email protected]