| First Author | Wang HC | Year | 2024 |
| Journal | Cell Rep | Volume | 43 |
| Issue | 8 | Pages | 114612 |
| PubMed ID | 39110592 | Mgi Jnum | J:353607 |
| Mgi Id | MGI:7716336 | Doi | 10.1016/j.celrep.2024.114612 |
| Citation | Wang HC, et al. (2024) Degraded tactile coding in the Cntnap2 mouse model of autism. Cell Rep 43(8):114612 |
| abstractText | 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. |
