title: Optogenetic Activation of Normalization in Alert Macaque Visual Cortex.
abstract: Normalization has been proposed as a canonical computation that accounts for a variety of nonlinear neuronal response properties associated with sensory processing and higher cognitive functions. A key premise of normalization is that the excitability of a neuron is inversely proportional to the overall activity level of the network. We tested this by optogenetically activating excitatory neurons in alert macaque primary visual cortex and measuring changes in neuronal activity as a function of stimulation intensity, with or without variable-contrast visual stimulation. Optogenetic depolarization of excitatory neurons either facilitated or suppressed baseline activity, consistent with indirect recruitment of inhibitory networks. As predicted by the normalization model, neurons exhibited sub-additive responses to optogenetic and visual stimulation, which depended lawfully on stimulation intensity and luminance contrast. We conclude that the normalization computation persists even under the artificial conditions of optogenetic stimulation, underscoring the canonical nature of this form of neural computation.
authors.affiliation: Systems Neurobiology Laboratories, Salk Institute for Biological Studies, La Jolla, CA 92037, USA. Electronic address: nassi@snl.salk.edu.
authors.forename: Jonathan J
authors.initials: JJ
authors.lastname: Nassi
authors.affiliation: Systems Neurobiology Laboratories, Salk Institute for Biological Studies, La Jolla, CA 92037, USA.
authors.forename: Michael C
authors.initials: MC
authors.lastname: Avery
authors.affiliation: Systems Neurobiology Laboratories, Salk Institute for Biological Studies, La Jolla, CA 92037, USA.
authors.forename: Ali H
authors.initials: AH
authors.lastname: Cetin
authors.affiliation: Department of Psychology, Vanderbilt University, Nashville, TN 37203, USA; Zhejiang University Interdisciplinary Institute of Neuroscience and Technology (ZIINT), Zhejiang University, 310027 Hangzhou, China.
authors.forename: Anna W
authors.initials: AW
authors.lastname: Roe
authors.affiliation: Systems Neurobiology Laboratories, Salk Institute for Biological Studies, La Jolla, CA 92037, USA.
authors.forename: John H
authors.initials: JH
authors.lastname: Reynolds
mesh_terms: D000818:Animals; D001931:Brain Mapping; D064032:Calbindin 2 / Q000378:metabolism; D064026:Calbindins / Q000378:metabolism; D002118:Calcium / Q000378:metabolism; D054729:Calcium-Calmodulin-Dependent Protein Kinase Type 1 / Q000235:genetics / Q000378:metabolism; D005071:Evoked Potentials / Q000502:physiology; D008164:Luminescent Proteins / Q000235:genetics; D008253:Macaca mulatta; D008297:Male; D008959:Models, Neurological; D009474:Neurons / Q000502:physiology*; D062308:Optogenetics; D010320:Parvalbumins / Q000378:metabolism; D010775:Photic Stimulation; D011930:Reaction Time / Q000502:physiology; D014793:Visual Cortex / Q000166:cytology* / Q000502:physiology*; D014796:Visual Perception
chemical_list: D064032:Calbindin 2; D064026:Calbindins; D008164:Luminescent Proteins; D010320:Parvalbumins; D054729:Calcium-Calmodulin-Dependent Protein Kinase Type 1; D002118:Calcium