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Channelrhodopsin as a tool to investigate synaptic transmission and plasticity
The light‐gated cation channel channelrhodopsin‐2 (ChR2) has been used in a variety of model systems to investigate the function of complex neuronal networks by stimulation of genetically targeted neurons. In slice physiology, ChR2 opens the door to novel types of experiments and greatly extends the...
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Published in: | Experimental physiology 2011-01, Vol.96 (1), p.34-39 |
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Main Authors: | , , |
Format: | Article |
Language: | English |
Subjects: | |
Citations: | Items that this one cites Items that cite this one |
Online Access: | Request full text |
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Summary: | The light‐gated cation channel channelrhodopsin‐2 (ChR2) has been used in a variety of model systems to investigate the function of complex neuronal networks by stimulation of genetically targeted neurons. In slice physiology, ChR2 opens the door to novel types of experiments and greatly extends the technical possibilities offered by traditional electrophysiology. In this short review, we first consider several technical aspects concerning the use of ChR2 in slice physiology, providing examples from our own work. More specifically, we discuss differences between light‐evoked action potentials and spontaneous or electrically induced action potentials. Our work implies that light‐evoked action potentials are associated with increased calcium influx and a very high probability of neurotransmitter release. Furthermore, we point out the factors limiting the spatial resolution of ChR2 activation. Secondly, we discuss how synaptic transmission and plasticity can be studied using ChR2. Postsynaptic depolarization induced by ChR2 can be combined with two‐photon glutamate uncaging to potentiate visually identified dendritic spines. ChR2‐mediated stimulation of presynaptic axons induces neurotransmitter release and reliably activates postsynaptic spines. In conclusion, ChR2 is a powerful tool to investigate activity‐dependent changes in structure and function of synapses. |
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ISSN: | 0958-0670 1469-445X |
DOI: | 10.1113/expphysiol.2009.051219 |