• Hiroyuki Arakawa.
• Department of Anatomy and Neurobiology, University of Maryland School of Medicine, Baltimore, MD, USA; Rodent Behavioral Core Department of Research Administration, Case Western Reserve University School of Medicine, Cleveland, OH, USA. Electronic address: harakawa@som.umaryland.edu.
• Neuroscience. 2020 Oct 1; 445: 144162144-162.

AbstractAutism is a complex spectrum of disorders characterized by core behavioral deficits in social communicative behavior, which are also required for comprehensive analysis of preclinical mouse models. As animal models of the core behavioral deficits in autism, two inbred mouse strains, BTBR T+ Itpr3tf/J (BTBR) and BALB/cJ (BALB), were compared with the standard social strain, C57BL/6J (B6), regarding a variety of behavioral factors underlying social communicative interactions, including olfactory and tactile sensory processes, social recognition abilities and behavioral expression strategies. Although both female BTBR and BALB mice can express social recognition and approach behavior depending on the stimuli they encounter, the available sensory modalities, along with modulation of the serotonergic system, differ between the two strains. BALB mice have deficits in using volatile olfactory cues and tactile information in a social context; they fail to exhibit a social approach to volatile cues and seek nonvolatile cues by exhibiting substantial sniff/contact behavior when allowed direct contact with social opponents. Systemic injection of the serotonin (5-HT1A) agonist buspirone has little effect on these social deficits, suggesting a congenitally degraded serotonergic system in BALB mice. In contrast, BTBR mice exhibit impaired body coordination and social motivation-modified olfactory signals, which are relevant to a reduced social approach. A systemic injection of the 5-HT1A agonist restored these social deficits in BTBR mice, indicating that a downregulated serotonergic system is involved in the social deficits exhibited by BTBR mice.Copyright © 2020 IBRO. Published by Elsevier Ltd. All rights reserved.

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