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Review
. 2013 Nov;34(11):1381-5.
doi: 10.1038/aps.2013.150. Epub 2013 Oct 28.

Optogenetics and synaptic plasticity

Affiliations
Review

Optogenetics and synaptic plasticity

Yu-feng Xie et al. Acta Pharmacol Sin. 2013 Nov.

Abstract

The intricate and complex interaction between different populations of neurons in the brain has imposed limits on our ability to gain detailed understanding of synaptic transmission and its integration when employing classical electrophysiological approaches. Indeed, electrical field stimulation delivered via traditional microelectrodes does not permit the targeted, precise and selective control of neuronal activity amongst a varied population of neurons and their inputs (eg, cholinergic, dopaminergic or glutamatergic neurons). Recently established optogenetic techniques overcome these limitations allowing precise control of the target neuron populations, which is essential for the elucidation of the neural substrates underlying complex animal behaviors. Indeed, by introducing light-activated channels (ie, microbial opsin genes) into specific neuronal populations, optogenetics enables non-invasive optical control of specific neurons with milliseconds precision. These approaches can readily be applied to freely behaving live animals. Recently there is increased interests in utilizing optogenetics tools to understand synaptic plasticity and learning/memory. Here, we summarize recent progress in applying optogenetics in in the study of synaptic plasticity.

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Figures

Figure 1
Figure 1
The NMDAR-dependent LTP and LTD induced by different electrical stimulation protocols. Inserts represent fEPSP before (1) and after (2) electrical stimulation at different frequencies.
Figure 2
Figure 2
The schematic structures (A) and spectrum activation (B) of ChR2, NpHR, and Arch.

References

    1. Xie YF, Belrose JC, Lei G, Tymianski M, Mori Y, MacDonald JF, et al. Dependence of NMDA/GSK-3beta mediated metaplasticity on TRPM2 channels at hippocampal CA3-CA1 synapses. Mol Brain. 2011;4:44. - PMC - PubMed
    1. Liu L, Wong TP, Pozza MF, Lingenhoehl K, Wang Y, Sheng M, et al. Role of NMDA receptor subtypes in governing the direction of hippocampal synaptic plasticity. Science. 2004;304:1021–4. - PubMed
    1. Morishita W, Lu W, Smith GB, Nicoll RA, Bear MF, Malenka RC. Activation of NR2B-containing NMDA receptors is not required for NMDA receptor-dependent long-term depression. Neuropharmacology. 2007;52:71–6. - PubMed
    1. Yang K, Trepanier C, Sidhu B, Xie YF, Li H, Lei G, et al. Metaplasticity gated through differential regulation of GluN2A versus GluN2B receptors by Src family kinases. EMBO J. 2012;31:805–16. - PMC - PubMed
    1. Henderson JM, Federici T, Boulis N. Optogenetic neuromodulation. Neurosurgery. 2009;64:796–804. - PubMed

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