Neural circuits underlying a psychotherapeutic regimen for fear disorders

Jinhee Baek, Sukchan Lee, Taesup Cho, Seong-Wook Kim, Minsoo Kim, Yongwoo Yoon, Ko Keun Kim, Junweon Byun, Sang Jeong Kim, Jaeseung Jeong () and Hee-Sup Shin ()
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Jinhee Baek: Center for Cognition and Sociality, Institute for Basic Science (IBS)
Sukchan Lee: Center for Cognition and Sociality, Institute for Basic Science (IBS)
Taesup Cho: Center for Cognition and Sociality, Institute for Basic Science (IBS)
Seong-Wook Kim: Center for Cognition and Sociality, Institute for Basic Science (IBS)
Minsoo Kim: Center for Cognition and Sociality, Institute for Basic Science (IBS)
Yongwoo Yoon: Center for Cognition and Sociality, Institute for Basic Science (IBS)
Ko Keun Kim: Center for Cognition and Sociality, Institute for Basic Science (IBS)
Junweon Byun: Center for Cognition and Sociality, Institute for Basic Science (IBS)
Sang Jeong Kim: Seoul National University College of Medicine
Jaeseung Jeong: Korea Advanced Institute of Science and Technology (KAIST)
Hee-Sup Shin: Center for Cognition and Sociality, Institute for Basic Science (IBS)

Nature, 2019, vol. 566, issue 7744, 339-343

Abstract: Abstract A psychotherapeutic regimen that uses alternating bilateral sensory stimulation (ABS) has been used to treat post-traumatic stress disorder. However, the neural basis that underlies the long-lasting effect of this treatment—described as eye movement desensitization and reprocessing—has not been identified. Here we describe a neuronal pathway driven by the superior colliculus (SC) that mediates persistent attenuation of fear. We successfully induced a lasting reduction in fear in mice by pairing visual ABS with conditioned stimuli during fear extinction. Among the types of visual stimulation tested, ABS provided the strongest fear-reducing effect and yielded sustained increases in the activities of the SC and mediodorsal thalamus (MD). Optogenetic manipulation revealed that the SC–MD circuit was necessary and sufficient to prevent the return of fear. ABS suppressed the activity of fear-encoding cells and stabilized inhibitory neurotransmission in the basolateral amygdala through a feedforward inhibitory circuit from the MD. Together, these results reveal the neural circuit that underlies an effective strategy for sustainably attenuating traumatic memories.

Date: 2019
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DOI: 10.1038/s41586-019-0931-y

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