美国研究人员利用一种新开发的技术：光遗传学（optogenetics）——结合遗传工程与光来操作个别神经细胞的活性，发现脑部如何产生γ波（gamma oscillations），并为它们在调控脑部功能中的角色提供新证据，这将有助于发展一系列脑相关失调的新疗法。
研究人员表示，“研究表明在罹患精神分裂症与其他精神病学与神经病学疾病的患者身上（被扰乱）会出现γ波，这种新工具给予我们很大的机会来探索这些信号通路的功能。”
γ振荡反映出大型互连神经元网路的同步活动，以范围在每秒 20 - 80 週期的频率发射。这些振荡被认为由一种特殊的抑制细胞（inhibitory cells）称为快闪中间神经元（fast-spiking interneurons） 所控制，但是到目前为止，这一设想并未得到具体的证实。
为了测定哪些神经元负责驱动这种振荡，研究人员利用一种被称为 channelrhodopsin-2（ChR2，第二型离子通道视紫质）的蛋白，这种蛋白能使神经元对光敏感。通过结合遗传学技术，研究人员在不同类型的神经元中表达了ChR2，通过激光与遍及脑部的光纤，精确调控它们的活性。
通过更进一步的实验，研究人员还发现根据刺激发生在振荡周期的哪个阶段，脑部对于触觉刺激的反应会更大或更小。从而支持了前文的构想：这些同步振荡对于控制我们如何感知刺激很重要。（生物谷Bioon.com）
生物谷推荐原始出处：
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.
