A Red Shifted Variant Of Channelrhodopsin Allows Deep Transcranial Optogenetic Excitation

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Lin, J.Y., Magne Knutsen, P., Muller, A., Kleinfeld, D., Tsien, R.Y. (2013) ReaChR: a red-shifted variant of channelrhodopsin enables deep transcranial optogenetic excitation. Nature neuroscience, 16 (10), 1499-1507.
This paper focusing on a res-shifted variant of Channelrhodopsin shows that using red light can improve transcranial excitation because of the properties of red light. Red light is less scattered by tissue and is absorbed less by blood than previously used wavelengths. This development is very important for the potential use of optogenetics in chronic studies to treat neurological disorders, as cranial windows can be avoided. The opsin created is called ReaChR and has a spectral response to light at wavelengths greater than
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Raimondo, J.V., Kay, L., Ellender, T.J., Akerman, C.J. (2012) Optogenetic silencing strategies differ in their effects on inhibitory transmission. Nature neuroscience, 15(8), 1102-1104.
It is important to know that optogenetic silencers can have different effects on synaptic transmission. For example, a light-driven inward Cl-pump, NpHR, causes changes in the reversal potential of the membrane potential of GABA receptors causing a spike after illumination. Arch, also an inward Cl- pump, on the other hand does not result in a spike after illumination. This article provides useful insight of light-activated proteins that can be used as modulators. The ability to change GABA membrane potential can be extremely useful when working with Parkinson models since these receptors are involved in some of the Parkinson’s symptoms.
Tønnesen, J. et al. (2011) Functional Integration of Grafted Neural Stem Cell-Derived Dopaminergic Neurons Monitored by Optogenetics in an In Vitro Parkinson Model. PlosOne, 6(3), 1-10
Intrastriatal grafts of stem cell-derived dopamine neurons induce behavioral recovery in animal models of Parkinson’s disease. This could possibly be used in non-animal models, however previously it was unknown how these transplanted grafts integrated in the host circuitry. By using optogenetic activation of grafted cells and inhibition of host neurons, Tønnesen and colleagues were able to

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