Prefrontal circuits guiding social preference: Implications in autism spectrum disorder

Fortier, Abigail V.; Meisner, Olivia; Nair, Amrita; Chang, Steve

doi:10.1016/j.neubiorev.2022.104803

Cited by 13 publications

(7 citation statements)

References 167 publications

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“… 76 Apart from the hippocampus, the prefrontal cortex is considered a key social hub involved in anxiety regulation and social preference. 77 , 78 In the present study, we showed that VPA mice exhibited reduced dendritic complexity, dendritic length, and branch point number in both the hippocampus and prefrontal cortex ( Figure 2 ). Moreover, there was a notable decrease in the number of synaptic spines in the VPA mice ( Figure 3 ).…”

Section: Discussionsupporting

confidence: 57%

Enhancing social behavior in an autism spectrum disorder mouse model: investigating the underlying mechanisms of Lactiplantibacillus plantarum intervention

Chen,

Wu,

Kim

et al. 2024

Gut Microbes

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Section: Discussionsupporting

confidence: 57%

Enhancing social behavior in an autism spectrum disorder mouse model: investigating the underlying mechanisms of Lactiplantibacillus plantarum intervention

Chen,

Wu,

Kim

et al. 2024

Gut Microbes

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“…Our findings of altered circuit dynamics in double Grin1 gene knockout in the BLA and mPFC would provide crucial insight into cognitive dysfunction, psychosis, and other psychiatric disorders such as autism spectrum disorder, 90 posttraumatic disorder (PTSD), 91 , 92 , 93 , 94 and schizophrenia. 95 The genetic toolbox applied in the current study is adequately applicable for understanding the operating principles of brain circuits for the various neurobiological processes and pathological conditions and has the potential to facilitate the design of circuit-targeted therapeutics to treat brain diseases.…”

Section: Discussionmentioning

confidence: 93%

Pre- and postsynaptic N-methyl-D-aspartate receptors are required for sequential printing of fear memory engrams

Bertocchi,

Rocha-Almeida,

Romero-Barragán

et al. 2023

iScience

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“…We found both male and female BDNF +/Met mice displayed significantly decreased time spent with social stimulus and social preference index, which confirmed that diminished activity-dependent BDNF is a common pathway in males and females of ASD. The prefrontal cortex (PFC), a hub brain region, is critical for “high level” executive functions, including working memory, sustained attention, and social communication ( 50 , 51 ), which is impaired in ASD patients and mouse models of autism ( 12 , 18 ). The autism-like social behavioral deficits are likely linked to diminished activity-dependent BDNF signaling in PFC.…”

Section: Discussionmentioning

confidence: 99%

Diminished activity-dependent BDNF signaling differentially causes autism-like behavioral deficits in male and female mice

Taylor

Williamson

et al. 2023

Front. Psychiatry

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Autism spectrum disorder (ASD) is a group of neurodevelopmental disorders with strong genetic heterogeneity and more prevalent in males than females. Recent human genetic studies have identified multiple high-risk genes for ASD, which produce similar phenotypes, indicating that diverse genetic factors converge to common molecular pathways. We and others have hypothesized that activity-dependent neural signaling is a convergent molecular pathway dysregulated in ASD. However, the causal link between diminished activity-dependent neural signaling and ASD remains unclear. Brain-derived neurotrophic factor (BDNF) is a key molecule mediating activity-dependent neural signaling. We therefore hypothesize that diminished activity-dependent BDNF signaling could confer autism-like behavioral deficits. Here, we investigated the effect of diminished activity-dependent BDNF signaling on autism-like behavioral deficits by using mice with genetic knock-in of a human BDNF methionine (Met) allele, which has decreased activity-dependent BDNF release without altering basal BDNF level. Compared with wild-type (WT) controls, diminished activity-dependent BDNF signaling similarly induced anxiety-like behaviors in male and female mice. Notably, diminished activity-dependent BDNF signaling differentially resulted in autism-like social deficits and increased self-grooming in male and female mice, and male mice were more severe than female mice. Again, sexually dimorphic spatial memory deficits were observed in female BDNF+/Met mice, but not in male BDNF+/Met mice. Our study not only reveals a causal link between diminished activity-dependent BDNF signaling and ASD-like behavioral deficits, but also identifies previously underappreciated sex-specific effect of diminished activity-dependent BDNF signaling in ASD. These mice with genetic knock-in of the human BDNF Met variant provide a distinct mouse model for studying the cellular and molecular mechanisms underlying diminished activity-dependent neural signaling, the common molecular pathway dysregulated in ASD.

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Prefrontal circuits guiding social preference: Implications in autism spectrum disorder

Cited by 13 publications

References 167 publications

Enhancing social behavior in an autism spectrum disorder mouse model: investigating the underlying mechanisms of Lactiplantibacillus plantarum intervention

Enhancing social behavior in an autism spectrum disorder mouse model: investigating the underlying mechanisms of Lactiplantibacillus plantarum intervention

Pre- and postsynaptic N-methyl-D-aspartate receptors are required for sequential printing of fear memory engrams

Diminished activity-dependent BDNF signaling differentially causes autism-like behavioral deficits in male and female mice

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