Again, a prestimulus baseline measurement (the mean of 1 s of data before the stimulus) was subtracted from the Z score. We would like to thank Eric Behnke and Tony Fields for technical assistance and Nanthia Suthana for electrode localizations. This work was supported by a grant from the National Institutes of Health (NS033221) as well as a University of California President’s Postdoctoral Fellowship (awarded to B.A.L.). “
“(Neuron 75, 1114–1121; September 20, 2012) As the result of a journal GSK1349572 clinical trial error during the production process, an incorrect version of the Supplemental Information was previously published

with this article online. We have now corrected the online Supplemental Information and apologize for the error. “
“(Neuron 79, 1–14; July 24, 2013) On page 8, the text mistakenly reads, “The fact that marked plasticity of ensemble plasticity appeared in both depth levels of IL only during the critical overtraining period in which habits became crystallized suggested an unexpected role of IL in the formation Fasudil order of habits, not only in their expression.” This text should instead read, “The fact that marked plasticity of ensemble activity appeared in both depth levels of IL only during the critical overtraining period in which habits became crystallized suggested an unexpected

role of IL in the formation of habits, not only in their expression.” This error has been corrected in the printed and online versions of the paper. “
“Optogenetics has revolutionized neuroscience through the use of heterologously expressed light-sensitive opsins that are G protein-coupled receptors, ion channels, or pumps to stimulate or inhibit activity in genetically selected neurons and brain regions, opening exciting avenues to probe the role of those cells in circuit

function and behavior (Szobota and Isacoff, 2010, Miesenböck, 2011 and Yizhar et al., 2011). In addition to naturally light-sensitive opsins used in “classical” optogenetics, chemical synthesis combined with protein engineering has produced a complementary “chemical” optogenetics, or photopharmacology, out in which native mammalian channels, as well as ionotropic and metabotropic receptors, can be blocked, agonized, or antagonized by light, enabling presynaptic or postsynaptic neuronal responses to neurotransmitter release to be selectively controlled (Kramer et al., 2013 and Levitz et al., 2013). While the optical activation of presynaptic rhodopsin can partially inhibit transmitter release during illumination (Li et al., 2005) and a light-activated metabotropic glutamate receptor can do so and persist for many minutes in the dark (Levitz et al., 2013) and both can be rapidly turned off, a method for ablation of neurotransmitter release that lasts for many hours has been missing from the optogenetic quiver.