Oxytocin attenuates deficits in social interaction but not recognition memory in a prenatal valproic acid-induced mouse model of autism

2017 ◽  
Vol 96 ◽  
pp. 130-136 ◽  
Author(s):  
Yuta Hara ◽  
Yukio Ago ◽  
Momoko Higuchi ◽  
Shigeru Hasebe ◽  
Takanobu Nakazawa ◽  
...  
2015 ◽  
Vol 9 (9) ◽  
pp. 926-939 ◽  
Author(s):  
Yuta Hara ◽  
Yukio Ago ◽  
Atsuki Taruta ◽  
Keisuke Katashiba ◽  
Shigeru Hasebe ◽  
...  

2019 ◽  
Vol 176 ◽  
pp. 1-5 ◽  
Author(s):  
Haruki Kawase ◽  
Yukio Ago ◽  
Megumi Naito ◽  
Momoko Higuchi ◽  
Yuta Hara ◽  
...  

2020 ◽  
Author(s):  
Irene Mollinedo-Gajate ◽  
Chenchen Song ◽  
Marcos Sintes-Rodriguez ◽  
Tobias Whelan ◽  
Anaïs Soula ◽  
...  

AbstractAutism spectrum disorder (ASD) is characterized by core deficits in social interaction. The classic serotonergic psychedelic psilocybin has been suggested as a therapeutic agent that may ameliorate in the core symptomology of ASD. We found that the acute response to psilocybin was attenuated in the prenatal valproic acid exposure mouse model of ASD, and importantly, psilocybin rescued the social behavioural abnormalities present in these ASD model mice.


Neuroscience ◽  
2020 ◽  
Vol 435 ◽  
pp. 22-32
Author(s):  
Roberta De Simone ◽  
Alessia Butera ◽  
Monica Armida ◽  
Antonella Pezzola ◽  
Monica Boirivant ◽  
...  

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Kana Okada ◽  
Kayo Nishizawa ◽  
Tomoko Kobayashi ◽  
Shogo Sakata ◽  
Kouichi Hashimoto ◽  
...  

AbstractSocial behaviour is a complex construct that is reported to include several components of social approach, interaction and recognition memory. Alzheimer’s disease (AD) is mainly characterized by progressive dementia and is accompanied by cognitive impairments, including a decline in social ability. The cholinergic system is a potential constituent for the neural mechanisms underlying social behaviour, and impaired social ability in AD may have a cholinergic basis. However, the involvement of cholinergic function in social behaviour has not yet been fully understood. Here, we performed a selective elimination of cholinergic cell groups in the basal forebrain in mice to examine the role of cholinergic function in social interaction and social recognition memory by using the three-chamber test. Elimination of cholinergic neurons in the medial septum (MS) and vertical diagonal band of Broca (vDB) caused impairment in social interaction, whereas ablating cholinergic neurons in the nucleus basalis magnocellularis (NBM) impaired social recognition memory. These impairments were restored by treatment with cholinesterase inhibitors, leading to cholinergic system activation. Our findings indicate distinct roles of MS/vDB and NBM cholinergic neurons in social interaction and social recognition memory, suggesting that cholinergic dysfunction may explain social ability deficits associated with AD symptoms.


2018 ◽  
Vol 115 (42) ◽  
pp. 10744-10749 ◽  
Author(s):  
Wei-Hsiang Huang ◽  
David C. Wang ◽  
William E. Allen ◽  
Matthew Klope ◽  
Hailan Hu ◽  
...  

Haploinsufficiency of Retinoic Acid Induced 1 (RAI1) causes Smith–Magenis syndrome (SMS), a syndromic autism spectrum disorder associated with craniofacial abnormalities, intellectual disability, and behavioral problems. There is currently no cure for SMS. Here, we generated a genetic mouse model to determine the reversibility of SMS-like neurobehavioral phenotypes in Rai1 heterozygous mice. We show that normalizing the Rai1 level 3–4 wk after birth corrected the expression of genes related to neural developmental pathways and fully reversed a social interaction deficit caused by Rai1 haploinsufficiency. In contrast, Rai1 reactivation 7–8 wk after birth was not beneficial. We also demonstrated that the correct Rai1 dose is required in both excitatory and inhibitory neurons for proper social interactions. Finally, we found that Rai1 heterozygous mice exhibited a reduction of dendritic spines in the medial prefrontal cortex (mPFC) and that optogenetic activation of mPFC neurons in adults improved the social interaction deficit of Rai1 heterozygous mice. Together, these results suggest the existence of a postnatal temporal window during which restoring Rai1 can improve the transcriptional and social behavioral deficits in a mouse model of SMS. It is possible that circuit-level interventions would be beneficial beyond this critical window.


2020 ◽  
Vol 11 (22) ◽  
pp. 3786-3792
Author(s):  
Kui Wang ◽  
Na Li ◽  
Min Xu ◽  
Meng Huang ◽  
Fei Huang

2018 ◽  
Vol 44 (3) ◽  
pp. 617-626 ◽  
Author(s):  
Sarah E. Scullion ◽  
Gareth R. I. Barker ◽  
E. Clea Warburton ◽  
Andrew D. Randall ◽  
Jonathan T. Brown

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