Light-Activated Learning
Ludwig-Maximillians-Universität | August 31, 2015
A German-French team has developed a light-sensitive switch that regulates a protein implicated in the neurobiology of synaptic plasticity. The agent promises to shed new light on the phenomenology of learning, memory and neurodegeneration.
Learning is made possible by the fact that the functional connections between nerve cells in the brain are subject to constant remodeling. As a result of activation-dependent modification of these links ('synaptic plasticity'), circuits that are repeatedly stimulated "learn" to transmit signals ever more efficiently.
<more at http://www.dddmag.com/news/2015/08/light-activated-learning; related links: http://www.uni-muenchen.de/forschung/news/2015/trauner_atg.html? (Lernen mit Licht. August 27, 2015) and http://www.nature.com/ncomms/2015/150827/ncomms9076/full/ncomms9076.html (Optical control of NMDA receptors with a diffusible photoswitch. Laura Laprell, Emilienne Repak, Vilius Franckevicius, Felix Hartrampf, Jan Terhag, Michael Hollmann, Martin Sumser, Nelson Rebola, David A. DiGregorio & Dirk Trauner. Nature Communications 6, Article number: 8076. doi:10.1038/ncomms9076. Published August 27, 2015. [Abstract: N-methyl-D-aspartate receptors (NMDARs) play a central role in synaptic plasticity, learning and memory, and are implicated in various neuronal disorders. We synthesized a diffusible photochromic glutamate analogue, azobenzene-triazole-glutamate (ATG), which is specific for NMDARs and functions as a photoswitchable agonist. ATG is inactive in its dark-adapted trans-isoform, but can be converted into its active cis-isoform using one-photon (near UV) or two-photon (740 nm) excitation. Irradiation with violet light photo-inactivates ATG within milliseconds, allowing agonist removal on the timescale of NMDAR deactivation. ATG is compatible with Ca2+ imaging and can be used to optically mimic synaptic coincidence detection protocols. Thus, ATG can be used like traditional caged glutamate compounds, but with the added advantages of NMDAR specificity, low antagonism of GABAR-mediated currents, and precise temporal control of agonist delivery.]>
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