Informational lesions: optical perturbation of spike timing and neural synchrony via microbial opsin gene fusions
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...
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| Format: | Article |
| Language: | en_US |
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Frontiers Research Foundation
2010
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| Online Access: | http://hdl.handle.net/1721.1/58588 https://orcid.org/0000-0002-8860-5914 https://orcid.org/0000-0002-0419-3351 |
| _version_ | 1810976262684934144 |
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| author | Han, Xue Qian, Xiaofeng Stern, Patrick Chuong, Amy S. Boyden, Edward |
| author2 | Massachusetts Institute of Technology. Department of Biological Engineering |
| author_facet | Massachusetts Institute of Technology. Department of Biological Engineering Han, Xue Qian, Xiaofeng Stern, Patrick Chuong, Amy S. Boyden, Edward |
| author_sort | Han, Xue |
| collection | MIT |
| description | 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. |
| first_indexed | 2024-09-23T08:52:29Z |
| format | Article |
| id | mit-1721.1/58588 |
| institution | Massachusetts Institute of Technology |
| language | en_US |
| last_indexed | 2024-09-23T08:52:29Z |
| publishDate | 2010 |
| publisher | Frontiers Research Foundation |
| record_format | dspace |
| spelling | mit-1721.1/585882022-09-30T11:48:37Z Informational lesions: optical perturbation of spike timing and neural synchrony via microbial opsin gene fusions Han, Xue Qian, Xiaofeng Stern, Patrick Chuong, Amy S. Boyden, Edward Massachusetts Institute of Technology. Department of Biological Engineering Massachusetts Institute of Technology. Department of Brain and Cognitive Sciences Massachusetts Institute of Technology. Department of Materials Science and Engineering Massachusetts Institute of Technology. Media Laboratory McGovern Institute for Brain Research at MIT Program in Media Arts and Sciences (Massachusetts Institute of Technology) Koch Institute for Integrative Cancer Research at MIT Boyden, Edward S. Han, Xue Qian, Xiaofeng Stern, Patrick Chuong, Amy S. Boyden, Edward Stuart optogenetics channelrhodopsin-2 halorhodopsin fusion protein synchrony 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. National Institutes of Health (U.S) (DP2 OD002002-01) National Science Foundation (U.S.) (0835878) National Science Foundation (U.S.) (0848804) McGovern Institute for Brain Research at MIT (Neurotechnology Award Program) United States. Dept. of Defense Alfred P. Sloan Foundation Jerry Burnett Foundation NARSAD (The Brain and Behavior Research Fund) Society for Neuroscience (Research Award for Innovation in Neuroscience) Massachusetts Institute of Technology. Media Laboratory Benesse Foundation Wallace H. Coulter Foundation Helen Hay Whitney Foundation National Institutes of Health (U.S) (1K99MH085944) 2010-09-17T17:53:36Z 2010-09-17T17:53:36Z 2009-07 2009-08 Article http://purl.org/eprint/type/JournalArticle 1662-5099 http://hdl.handle.net/1721.1/58588 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 https://orcid.org/0000-0002-8860-5914 https://orcid.org/0000-0002-0419-3351 en_US http://dx.doi.org/10.3389/neuro.02.012.2009 Frontiers in Molecular Neuroscience Article is made available in accordance with the publisher's policy and may be subject to US copyright law. Please refer to the publisher's site for terms of use. application/pdf Frontiers Research Foundation MIT Web Domain |
| spellingShingle | optogenetics channelrhodopsin-2 halorhodopsin fusion protein synchrony Han, Xue Qian, Xiaofeng Stern, Patrick Chuong, Amy S. Boyden, Edward Informational lesions: optical perturbation of spike timing and neural synchrony via microbial opsin gene fusions |
| title | Informational lesions: optical perturbation of spike timing and neural synchrony via microbial opsin gene fusions |
| title_full | Informational lesions: optical perturbation of spike timing and neural synchrony via microbial opsin gene fusions |
| title_fullStr | Informational lesions: optical perturbation of spike timing and neural synchrony via microbial opsin gene fusions |
| title_full_unstemmed | Informational lesions: optical perturbation of spike timing and neural synchrony via microbial opsin gene fusions |
| title_short | Informational lesions: optical perturbation of spike timing and neural synchrony via microbial opsin gene fusions |
| title_sort | informational lesions optical perturbation of spike timing and neural synchrony via microbial opsin gene fusions |
| topic | optogenetics channelrhodopsin-2 halorhodopsin fusion protein synchrony |
| url | http://hdl.handle.net/1721.1/58588 https://orcid.org/0000-0002-8860-5914 https://orcid.org/0000-0002-0419-3351 |
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