Page 32 - Q. Neuroscience

[Q. Neuroscience-18]

Disruption in cortical inputs to the posterior parietal cortex

and multisensory integration in Shank3Δ14–16 mice

You-Hyang Song¹˙#, Daun Jeong¹˙#, Jun-Ho Song², Jae-Hyun Kim¹, Taesun Yoo¹, Eunjoon Kim¹, Se-Bum Paik²,
Seung-Hee Lee¹˙*

¹Biological Sciences, KAIST, Daejeon 34141, 대한민국, ²Bio and Brain engineering, KAIST, Daejeon 34141, 대한민국

Sensory processing disorder (SPD) is a common symptom of autism. Genetic mutation of Shank3 causes autistic

and schizophrenic behaviors in both human and mice, but it is unclear whether this phenotype is correlated with
any changes in brain circuit wiring pattern or sensory-guided behaviors. Here, we examined whether cortical

circuits and perceptual behaviors are changed in mice deleted with Shank3 exons 14-16 (Shank3Δ14–16) compared
to the normal mice. We first mapped the cortical inputs to each sub-areas within the posterior parietal cortex (PPC)

in normal mice by quantifying the number of neurons throughout the brain labeled with rabies virus injected into
the PPC. We then compared this connectivity pattern in Shank3Δ14–16 mice. We found that Shank3Δ14–16 mice

show significantly reduced inputs to the VISa from the auditory cortex and the Cg/RSP areas. We further found that
Shank3Δ14–16 mice show weaker auditory dominance and less multisensory enhancement in the audiovisual

integration task with little changes in unisensory perceptual behaviors. Collectively, our data suggests that disrupted
cortical network in Shank3Δ14–16 mice leads to the impaired sensory integration during perceptual behaviors.