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Degraded tactile coding in the Cntnap2 mouse model of autism.
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- Author(s): Wang, Han; Wang, Han; Feldman, Daniel
- Source:
Cell Reports; vol 43, iss 8
- Document Type:
Electronic Resource
- Online Access:
https://escholarship.org/uc/item/2qw0s3ct
https://escholarship.org/content/qt2qw0s3ct/qt2qw0s3ct.pdf
- Additional Information
- Publisher Information:
eScholarship, University of California 2024-08-27
- Abstract:
Atypical sensory processing is common in autism, but how neural coding is disrupted in sensory cortex is unclear. We evaluate whisker touch coding in L2/3 of somatosensory cortex (S1) in Cntnap2-/- mice, which have reduced inhibition. This classically predicts excess pyramidal cell spiking, but this remains controversial, and other deficits may dominate. We find that c-fos expression is elevated in S1 of Cntnap2-/- mice under spontaneous activity conditions but is comparable to that of control mice after whisker stimulation, suggesting normal sensory-evoked spike rates. GCaMP8m imaging from L2/3 pyramidal cells shows no excess whisker responsiveness, but it does show multiple signs of degraded somatotopic coding. This includes broadened whisker-tuning curves, a blurred whisker map, and blunted whisker point representations. These disruptions are greater in noisy than in sparse sensory conditions. Tuning instability across days is also substantially elevated in Cntnap2-/-. Thus, Cntnap2-/- mice show no excess sensory-evoked activity, but a degraded and unstable tactile code in S1.
- Subject Terms:
- Availability:
Open access content. Open access content
public
- Note:
application/pdf
Cell Reports vol 43, iss 8
- Other Numbers:
CDLER oai:escholarship.org:ark:/13030/qt2qw0s3ct
qt2qw0s3ct
https://escholarship.org/uc/item/2qw0s3ct
https://escholarship.org/content/qt2qw0s3ct/qt2qw0s3ct.pdf
info:doi/10.1016/j.celrep.2024.114612
https://escholarship.org/
1468512127
- Contributing Source:
UC MASS DIGITIZATION
From OAIster®, provided by the OCLC Cooperative.
- Accession Number:
edsoai.on1468512127
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