This article is part of the Research Topic Genetic techniques and circuit analysis

Perspective ARTICLE

Front. Mol. Neurosci., 27 August 2009 | doi: 10.3389/neuro.02.012.2009

Informational lesions: optical perturbation of spike timing and neural synchrony via microbial opsin gene fusions

1
MIT Media Lab, Massachusetts Institute of Technology, Cambridge, MA, USA
2
Brain and Cognitive Sciences, Massachusetts Institute of Technology, Cambridge, MA, USA
3
McGovern Institute, Massachusetts Institute of Technology, Cambridge, MA, USA
4
Koch Center for Cancer Research, Massachusetts Institute of Technology, Cambridge, MA, USA
5
Biological Engineering, Massachusetts Institute of Technology, Cambridge, MA, USA
Synchronous neural activity occurs throughout the brain in association with normal and pathological brain functions. Despite theoretical work exploring how such neural coordination might facilitate neural computation and be corrupted in disease states, it has proven difficult to test experimentally the causal role of synchrony in such phenomena. Attempts to manipulate neural synchrony often alter other features of neural activity such as firing rate. Here we evaluate a single gene which encodes for the blue-light gated cation channel channelrhodopsin-2 and the yellow-light driven chloride pump halorhodopsin from Natronobacterium pharaonis, linked by a ‘self-cleaving’ 2A peptide. This fusion enables proportional expression of both opsins, sensitizing neurons to being bi-directionally controlled with blue and yellow light, facilitating proportional optical spike insertion and deletion upon delivery of trains of precisely-timed blue and yellow light pulses. Such approaches may enable more detailed explorations of the causal role of specific features of the neural code.
Keywords:
optogenetics, channelrhodopsin-2, halorhodopsin, fusion protein, synchrony
Citation:
Han X, Qian X, Stern P, Chuong AS and Boyden ES (2009). Informational lesions: optical perturbation of spike timing and neural synchrony via microbial opsin gene fusions. Front. Mol. Neurosci. 2:12. doi: 10.3389/neuro.02.012.2009
Received:
07 July 2009;
 Paper pending published:
21 July 2009;
Accepted:
10 August 2009;
 Published online:
27 August 2009.

Edited by:

Jochen C. Meier, Max Delbrück Center for Molecular Medicine, Germany

Reviewed by:

Miles A. Whittington, Newcastle University, UK
Antoine Adamantidis, Stanford University School of Medicine, USA
Copyright:
© 2009 Han, Qian, Stern, Chuong and Boyden. This is an open-access article subject to an exclusive license agreement between the authors and the Frontiers Research Foundation, which permits unrestricted use, distribution, and reproduction in any medium, provided the original authors and source are credited.
*Correspondence:
Edward S. Boyden, MIT Media Lab, E15-430, 20 Ames St., Cambridge, MA 02139, USA. e-mail: edboyden@mit.edu
Back to top