Journal
NEURON
Volume 87, Issue 3, Pages 605-620Publisher
CELL PRESS
DOI: 10.1016/j.neuron.2015.07.002
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Funding
- National Institute on Drug Abuse (NIDA) [R21 DA035144]
- McDonnell Center for Systems Neuroscience
- NIDA [R01 DA035821, K99 DA038725]
- NIMH [F31 MH101956]
- Washington University School of Medicine Division of Biological and Biomedical Sciences
- Washington University School of Medicine HOPE Center viral vector core (National Institute of Neurological Disorders and Stroke [NINDS]) [P30NS057105]
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The locus coeruleus noradrenergic (LC-NE) system is one of the first systems engaged following a stressful event. While numerous groups have demonstrated that LC-NE neurons are activated by many different stressors, the underlying neural circuitry and the role of this activity in generating stress-induced anxiety has not been elucidated. Using a combination of in vivo chemogenetics, optogenetics, and retrograde tracing, we determine that increased tonic activity of the LC-NE system is necessary and sufficient for stress-induced anxiety and aversion. Selective inhibition of LC-NE neurons during stress prevents subsequent anxiety-like behavior. Exogenously increasing tonic, but not phasic, activity of LC-NE neurons is alone sufficient for anxiety-like and aversive behavior. Furthermore, endogenous corticotropin-releasing hormone(+) (CRH+) LC inputs from the amygdala increase tonic LC activity, inducing anxiety-like behaviors. These studies position the LC-NE system as a critical mediator of acute stress-induced anxiety and offer a potential intervention for preventing stress-related affective disorders.
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