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Optogenetic Approaches to Understand the Neural Circuit Mechanism of Social Deficits Seen in Autism Spectrum Disorders

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Book cover Optogenetics

Part of the book series: Advances in Experimental Medicine and Biology ((AEMB,volume 1293))

Abstract

Individuals with neurodevelopmental disorders, such as autism spectrum disorders (ASDs), are diagnosed based on nonquantitative objective parameters such as behavioral phenotypes. It is still unclear how any neural mechanism affects such behavioral phenotypes in these patients. In human genetics, a large number of genetic abnormalities including single nucleotide variation (SNV) and copy number variation (CNV) have been found in individuals with ASDs. It is thought that influence of such variations converges on dysfunction of neural circuit resulting in common behavioral phenotypes of ASDs such as deficits in social communication and interaction. Recent studies suggest that an excitatory/inhibitory (E/I) imbalanced state, which induces disruption of neural circuit activities, is one of the pathophysiological abnormalities in ASD brains. To assess the causal relationship between brain abnormalities and behavioral deficits, we can take advantage of optogenetics with animal models of ASDs that recapitulate human genetic mutations. Here, we review optogenetics studies being utilized to dissect neural circuit mechanisms associated with social deficits in model mice of ASD. Optogenetic manipulation of disrupted neural activities would help us understand how neural circuits affect behavioral deficits observed in ASDs.

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Abbreviations

5-HT:

5-Hydroxytryptamine (serotonin)

ACC:

Anterior cingulate cortex

ASD:

Autism spectrum disorder

CMS:

Chronic mild stress

CNV:

Copy number variation

DBS:

Deep brain stimulation

DRN:

Dorsal raphe nucleus

E/I:

Excitatory/inhibitory

EEG:

Electroencephalography

GABA:

γ-Aminobutyric acid

GAD:

Glutamic acid decarboxylase

KI:

Knockin

KO:

Knockout

LFP:

Long-term potentiation

MEG:

Magnetoencephalography

mPFC:

Medial prefrontal cortex

NAc:

Nucleus accumbens

NMDAR:

N-methyl-d-aspartate receptor

NS:

Narrow-spiking

PL:

Prelimbic area

PV:

Parvalbumin

SDS:

Social defeat stress

SNV:

Single-nucleotide variation

SSFO:

Stable step-function opsin

VTA:

Ventral tegmental area

WS:

Wide-spiking

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Acknowledgments

This work was supported in part by KAKENHI (16H06316, 16H06463, 19K16886), Japan Society of Promotion of Science and Ministry of Education, Culture, Sports, Science, and Technology, Intramural Research Grant for Neurological and Psychiatric Disorders of NCNP, the Takeda Science Foundation, and the Smoking Science Foundation.

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Authors and Affiliations

  1. RIKEN Brain Science Institute, Wako, Saitama, Japan

    Nobuhiro Nakai, Eric T. N. Overton & Toru Takumi

  2. Department of Physiology and Cell Biology, Kobe University School of Medicine, Kobe , Japan

    Nobuhiro Nakai & Toru Takumi

Authors
  1. Nobuhiro Nakai
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  2. Eric T. N. Overton
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  3. Toru Takumi
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Correspondence to Toru Takumi .

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Editors and Affiliations

  1. The Institute for Solid State Physics, The University of Tokyo, Kashiwa, Japan

    Hiromu Yawo

  2. OptoBioTechnology Research Center, Nagoya Institute of Technology, Nagoya, Japan

    Hideki Kandori

  3. National Institutes of Natural Sciences, Tokyo, Japan

    Amane Koizumi

  4. Institute for Frontier Life and Medical Sciences, Kyoto University, Kyoto, Japan

    Ryoichiro Kageyama

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Nakai, N., Overton, E.T.N., Takumi, T. (2021). Optogenetic Approaches to Understand the Neural Circuit Mechanism of Social Deficits Seen in Autism Spectrum Disorders. In: Yawo, H., Kandori, H., Koizumi, A., Kageyama, R. (eds) Optogenetics. Advances in Experimental Medicine and Biology, vol 1293. Springer, Singapore. https://doi.org/10.1007/978-981-15-8763-4_36

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