Behavioral neuroscience of autism

Toru Takumi*, Kota Tamada, Fumiyuki Hatanaka, Nobuhiro Nakai, Patrick F. Bolton

*Corresponding author for this work

Research output: Contribution to journalReview articlepeer-review

70 Citations (Scopus)

Abstract

Autism spectrum disorder (ASD)is a neurodevelopmental disorder. Several genetic causes of ASD have been identified and this has enabled researchers to construct mouse models. Mouse behavioral tests reveal impaired social interaction and communication, as well as increased repetitive behavior and behavioral inflexibility in these mice, which correspond to core behavioral deficits observed in individuals with ASD. However, the connection between these behavioral abnormalities and the underlying dysregulation in neuronal circuits and synaptic function is poorly understood. Moreover, different components of the ASD phenotype may be linked to dysfunction in different brain regions, making it even more challenging to chart the pathophysiological mechanisms involved in ASD. Here we summarize the research on mouse models of ASD and their contribution to understanding pathophysiological mechanisms. Specifically, we emphasize abnormal serotonin production and regulation, as well as the disruption in circadian rhythms and sleep that are observed in a subset of ASD, and propose that spatiotemporal disturbances in brainstem development may be a primary cause of ASD that propagates towards the cerebral cortex.

Original languageEnglish
JournalNeuroscience and Biobehavioral Reviews
DOIs
Publication statusE-pub ahead of print - 3 May 2019

Keywords

  • 3-chamber test
  • ASD biology
  • Autism
  • Autism spectrum disorder
  • Behavior
  • Brainstem
  • Circadian rhythm
  • CNV
  • Dorsal raphe nuclei
  • Hindbrain
  • Mouse model
  • Neurodevelopmental disorder
  • PI3K-mTOR
  • Serotonin
  • Sleep
  • Social behavior
  • Somatosensory
  • Suprachiasmatic nucleus
  • Synapse
  • Ultrasonic vocalization

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