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5-HT release in nucleus accumbens rescues social deficits in mouse autism model

Author

Listed:
  • Jessica J. Walsh

    (Stanford University)

  • Daniel J. Christoffel

    (Stanford University)

  • Boris D. Heifets

    (Stanford University School of Medicine)

  • Gabriel A. Ben-Dor

    (Stanford University)

  • Aslihan Selimbeyoglu

    (Stanford University
    Stanford University
    Stanford University)

  • Lin W. Hung

    (Stanford University)

  • Karl Deisseroth

    (Stanford University
    Stanford University)

  • Robert C. Malenka

    (Stanford University)

Abstract

Dysfunction in prosocial interactions is a core symptom of autism spectrum disorder. However, the neural mechanisms that underlie sociability are poorly understood, limiting the rational development of therapies to treat social deficits. Here we show in mice that bidirectional modulation of the release of serotonin (5-HT) from dorsal raphe neurons in the nucleus accumbens bidirectionally modifies sociability. In a mouse model of a common genetic cause of autism spectrum disorder—a copy number variation on chromosome 16p11.2—genetic deletion of the syntenic region from 5-HT neurons induces deficits in social behaviour and decreases dorsal raphe 5-HT neuronal activity. These sociability deficits can be rescued by optogenetic activation of dorsal raphe 5-HT neurons, an effect requiring and mimicked by activation of 5-HT1b receptors in the nucleus accumbens. These results demonstrate an unexpected role for 5-HT action in the nucleus accumbens in social behaviours, and suggest that targeting this mechanism may prove therapeutically beneficial.

Suggested Citation

  • Jessica J. Walsh & Daniel J. Christoffel & Boris D. Heifets & Gabriel A. Ben-Dor & Aslihan Selimbeyoglu & Lin W. Hung & Karl Deisseroth & Robert C. Malenka, 2018. "5-HT release in nucleus accumbens rescues social deficits in mouse autism model," Nature, Nature, vol. 560(7720), pages 589-594, August.
  • Handle: RePEc:nat:nature:v:560:y:2018:i:7720:d:10.1038_s41586-018-0416-4
    DOI: 10.1038/s41586-018-0416-4
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    Cited by:

    1. Carole Morel & Sarah E. Montgomery & Long Li & Romain Durand-de Cuttoli & Emily M. Teichman & Barbara Juarez & Nikos Tzavaras & Stacy M. Ku & Meghan E. Flanigan & Min Cai & Jessica J. Walsh & Scott J., 2022. "Midbrain projection to the basolateral amygdala encodes anxiety-like but not depression-like behaviors," Nature Communications, Nature, vol. 13(1), pages 1-13, December.
    2. Hyosang Kim & Doyoun Kim & Yisul Cho & Kyungdeok Kim & Junyeop Daniel Roh & Yangsik Kim & Esther Yang & Seong Soon Kim & Sunjoo Ahn & Hyun Kim & Hyojin Kang & Yongchul Bae & Eunjoon Kim, 2022. "Early postnatal serotonin modulation prevents adult-stage deficits in Arid1b-deficient mice through synaptic transcriptional reprogramming," Nature Communications, Nature, vol. 13(1), pages 1-19, December.

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