Sensory Cortical Control of a Visually Induced Arrest Behavior via Corticotectal Projections.
Innate defense behaviors (IDBs) evoked by threatening sensory stimuli are essential for animal survival. Although subcortical circuits are implicated in IDBs, it remains largely unclear whether sensory cortex modulates IDBs and what the underlying neural pathways are. Here, we show that optogenetic silencing of corticotectal projections from layer 5 (L5) of the mouse primary visual cortex (V1) to the superior colliculus (SC) significantly reduces an SC-dependent innate behavior (i.e., temporary suspension of locomotion upon a sudden flash of light as short as milliseconds). Surprisingly, optogenetic activation of SC-projecting neurons in V1 or their axon terminals in SC sufficiently elicits the behavior, in contrast to other major L5 corticofugal projections. Thus, via the same corticofugal projection, visual cortex not only modulates the light-induced arrest behavior, but also can directly drive the behavior. Our results suggest that sensory cortex may play a previously unrecognized role in the top-down initiation of sensory-motor behaviors.
Zilkha Neurogenetic Institute, Keck School of Medicine, University of Southern California, Los Angeles, CA 90033, USA; Department of Cell and Neurobiology, Keck School of Medicine, University of Southern California, Los Angeles, CA 90033, USA.
Feixue
F
Liang
Zilkha Neurogenetic Institute, Keck School of Medicine, University of Southern California, Los Angeles, CA 90033, USA; Neuroscience Graduate Program, Keck School of Medicine, University of Southern California, Los Angeles, CA 90033, USA.
Xiaorui R
XR
Xiong
Zilkha Neurogenetic Institute, Keck School of Medicine, University of Southern California, Los Angeles, CA 90033, USA; Neuroscience Graduate Program, Keck School of Medicine, University of Southern California, Los Angeles, CA 90033, USA.
Brian
B
Zingg
Zilkha Neurogenetic Institute, Keck School of Medicine, University of Southern California, Los Angeles, CA 90033, USA; Department of Physiology, School of Basic Medical Sciences, Southern Medical University, Guangzhou 510515, China.
Xu-ying
XY
Ji
Zilkha Neurogenetic Institute, Keck School of Medicine, University of Southern California, Los Angeles, CA 90033, USA; Department of Physiology and Biophysics, Keck School of Medicine, University of Southern California, Los Angeles, CA 90033, USA. Electronic address: liizhang@usc.edu.
Li I
LI
Zhang
Zilkha Neurogenetic Institute, Keck School of Medicine, University of Southern California, Los Angeles, CA 90033, USA; Department of Cell and Neurobiology, Keck School of Medicine, University of Southern California, Los Angeles, CA 90033, USA. Electronic address: htao@usc.edu.
Huizhong W
HW
Tao
D000818:Animals; D000075402:Channelrhodopsins; D002772:Cholera Toxin / Q000493:pharmacokinetics; D005260:Female; D058785:GABA-A Receptor Agonists / Q000494:pharmacology; D066298:In Vitro Techniques; D007323:Instinct; D008027:Light; D008297:Male; D051379:Mice; D008810:Mice, Inbred C57BL; D009118:Muscimol / Q000494:pharmacology; D010446:Peptide Fragments / Q000493:pharmacokinetics; D010775:Photic Stimulation; D054839:Retinol-Binding Proteins, Plasma / Q000235:genetics / Q000378:metabolism; D013477:Superior Colliculi / Q000166:cytology / Q000502:physiology*; D014161:Transduction, Genetic; D050494:Vesicular Acetylcholine Transport Proteins / Q000235:genetics; D014793:Visual Cortex / Q000166:cytology / Q000502:physiology*; D014795:Visual Pathways / Q000502:physiology*; D014851:Wakefulness
D000075402:Channelrhodopsins; D058785:GABA-A Receptor Agonists; D010446:Peptide Fragments; C502487:Rbp4 protein, mouse; D054839:Retinol-Binding Proteins, Plasma; D050494:Vesicular Acetylcholine Transport Proteins; C084765:cholera toxin B subunit (50-75); D009118:Muscimol; D002772:Cholera Toxin