美國(guó)研究人員利用一種新開(kāi)發(fā)的技術(shù)：光遺傳學(xué)（optogenetics）——結(jié)合遺傳工程與光來(lái)操作個(gè)別神經(jīng)細(xì)胞的活性,，發(fā)現(xiàn)腦部如何產(chǎn)生γ波（gamma oscillations），并為它們?cè)谡{(diào)控腦部功能中的角色提供新證據(jù)，這將有助于發(fā)展一系列腦相關(guān)失調(diào)的新療法,。
研究人員表示,，“研究表明在罹患精神分裂癥與其他精神病學(xué)與神經(jīng)病學(xué)疾病的患者身上（被擾亂）會(huì)出現(xiàn)γ波，這種新工具給予我們很大的機(jī)會(huì)來(lái)探索這些信號(hào)通路的功能,。”
γ振蕩反映出大型互連神經(jīng)元網(wǎng)路的同步活動(dòng),，以范圍在每秒 20 - 80 週期的頻率發(fā)射。這些振蕩被認(rèn)為由一種特殊的抑制細(xì)胞（inhibitory cells）稱(chēng)為快閃中間神經(jīng)元（fast-spiking interneurons） 所控制,，但是到目前為止,，這一設(shè)想并未得到具體的證實(shí)。
為了測(cè)定哪些神經(jīng)元負(fù)責(zé)驅(qū)動(dòng)這種振蕩,，研究人員利用一種被稱(chēng)為 channelrhodopsin-2（ChR2,，第二型離子通道視紫質(zhì)）的蛋白，這種蛋白能使神經(jīng)元對(duì)光敏感,。通過(guò)結(jié)合遺傳學(xué)技術(shù),，研究人員在不同類(lèi)型的神經(jīng)元中表達(dá)了ChR2，通過(guò)激光與遍及腦部的光纖,，精確調(diào)控它們的活性,。
通過(guò)更進(jìn)一步的實(shí)驗(yàn)，研究人員還發(fā)現(xiàn)根據(jù)刺激發(fā)生在振蕩周期的哪個(gè)階段,，腦部對(duì)于觸覺(jué)刺激的反應(yīng)會(huì)更大或更小,。從而支持了前文的構(gòu)想：這些同步振蕩對(duì)于控制我們?nèi)绾胃兄碳ず苤匾＃ㄉ锕菳ioon.com）
生物谷推薦原始出處：
Nature advance online publication 26 April 2009 | doi:10.1038/nature08002
Driving fast-spiking cells induces gamma rhythm and controls sensory responses
Jessica A. Cardin1,2,7, Marie Carlén3,4,7, Konstantinos Meletis3,4, Ulf Knoblich1, Feng Zhang5, Karl Deisseroth5, Li-Huei Tsai3,4,6 & Christopher I. Moore1
1 McGovern Institute for Brain Research and Department of Brain and Cognitive Sciences, MIT, Cambridge, Massachusetts 02139, USA
2 Department of Neuroscience, University of Pennsylvania, Philadelphia, Pennsylvania 19104, USA
3 Picower Institute for Learning and Memory, Department of Brain and Cognitive Sciences, MIT, Cambridge, Massachusetts 02139, USA
4 Stanley Center for Psychiatric Research, Broad Institute of Harvard and Massachusetts Institute of Technology, Cambridge, Massachusetts 02139, USA
5 Department of Bioengineering, Stanford University, Stanford, California 94305, USA
6 Howard Hughes Medical Institute, Cambridge, Massachusetts 02139, USA
7 These authors contributed equally to this work.
Cortical gamma oscillations (20-80 Hz) predict increases in focused attention, and failure in gamma regulation is a hallmark of neurological and psychiatric disease. Current theory predicts that gamma oscillations are generated by synchronous activity of fast-spiking inhibitory interneurons, with the resulting rhythmic inhibition producing neural ensemble synchrony by generating a narrow window for effective excitation. We causally tested these hypotheses in barrel cortex in vivo by targeting optogenetic manipulation selectively to fast-spiking interneurons. Here we show that light-driven activation of fast-spiking interneurons at varied frequencies (8-200 Hz) selectively amplifies gamma oscillations. In contrast, pyramidal neuron activation amplifies only lower frequency oscillations, a cell-type-specific double dissociation. We found that the timing of a sensory input relative to a gamma cycle determined the amplitude and precision of evoked responses. Our data directly support the fast-spiking-gamma hypothesis and provide the first causal evidence that distinct network activity states can be induced in vivo by cell-type-specific activation.
