English (United Kingdom)

https://curated-unify.zendy.io/wp-json/zendy-region/v1/featured_content/oa?rat=en

https://curated-unify.zendy.io/wp-json/zendy-region/v1/highlighted_journal/

Global: Zendy Plus annual

Presents the access of premium content as premium feature

Premium Content

Presents the keyphrase highlighting as premium feature

Keyphrase Highlighting

Presents the summarisation as premium feature

Summarisation

Insights

Presents the pdf analysis as premium feature

PDF Analysis

Presents the zaia usage as premium feature

ZAIA

Global: Zendy Tools annual

Global: Zendy Free Plan

Global: Zendy Tools monthly

Global: Zendy Plus monthly

Sensory integration difficulties have been reported in autism, but their underlying brain-circuit mechanisms are underexplored. Using five autism-related mouse models,  Shank3+ /ΔC,  Mecp2  R308/Y ,  Cntnap2 −/−, L7-Tsc1 ( L7/Pcp2   Cre   ::Tsc1   flox/ + ), and patDp(15q11-13)/+, we report specific perturbations in delay eyeblink conditioning, a form of associative sensory learning requiring cerebellar plasticity. By distinguishing perturbations in the probability and characteristics of learned responses, we found that probability was reduced in  Cntnap2 −/−, patDp(15q11-13)/+, and  L7/Pcp2   Cre   ::Tsc1   flox/ + , which are associated with Purkinje-cell/deep-nuclear gene expression, along with  Shank3 +/ΔC. Amplitudes were smaller in  L7/Pcp2   Cre   ::Tsc1   flox/ +  as well as  Shank3 +/ΔC and  Mecp2  R308/Y , which are associated with granule cell pathway expression.  Shank3+ /ΔC and  Mecp2  R308/Y  also showed aberrant response timing and reduced Purkinje-cell dendritic spine density. Overall, our observations are potentially accounted for by defects in instructed learning in the olivocerebellar loop and response representation in the granule cell pathway. Our findings indicate that defects in associative temporal binding of sensory events are widespread in autism mouse models.

Cerebellar associative sensory learning defects in five mouse autism models