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Peer-reviewedCC BYNeuron

Cell-type-specific disruption of nucleus accumbens social representations in a mouse model of autism

  • Pingping Zhao1
  • Xing Chen1
  • Arash Bellafard1
  • Avaneesh Murugesan1
  • Jonathan Quan1
  • Daniel Aharoni1
  • Peyman Golshani
  1. 1Department of Neurology, David Geffen School of Medicine, University of California, Los Angeles, Los Angeles, CA, USA
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Abstract

How cell-type-specific nucleus accumbens (NAc) circuits encode social interactions, and whether this encoding is disrupted in autism spectrum disorder (ASD), remains unresolved. Using longitudinal miniscope calcium imaging and optogenetics in mice, we show that NAc core population activity selectively encodes social interaction and that NAc inhibition enhances sociability. In Cntnap2 −/− mice, both acute and cross-day social representations are degraded, and NAc inhibition persistently improves sociability. Cell-type-specific recordings and optogenetics reveal opposing medium spiny neuron (MSN) contributions: D1-MSNs promote sociability, and D2-MSNs suppress it. Cntnap2 −/− mice exhibit selective depletion of socially excited D1-MSNs and socially inhibited D2-MSNs, along with impaired cross-day population decoding. D2-MSN inhibition improves social behavior in Cntnap2 −/− mice, and D1-MSN activation does not. Together, these findings link disrupted, cell-type-specific NAc social representations to ASD-related social dysfunction and suggest that targeted modulation of NAc activity may improve social behavior.

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Cite

BibTeXRIS
BibTeX
@article{zhao2026celltypespecific,
  title = {{Cell-type-specific disruption of nucleus accumbens social representations in a mouse model of autism}},
  author = {Pingping Zhao and Xing Chen and Arash Bellafard and Avaneesh Murugesan and Jonathan Quan and Daniel Aharoni and Peyman Golshani},
  journal = {Neuron},
  year = {2026},
  month = sep,
  doi = {10.1016/j.neuron.2026.08.007},
  url = {https://doi.org/10.1016/j.neuron.2026.08.007},
  note = {CC BY},
}
RIS
TY  - JOUR
TI  - Cell-type-specific disruption of nucleus accumbens social representations in a mouse model of autism
AU  - Pingping Zhao
AU  - Xing Chen
AU  - Arash Bellafard
AU  - Avaneesh Murugesan
AU  - Jonathan Quan
AU  - Daniel Aharoni
AU  - Peyman Golshani
PY  - 2026
DA  - 2026/09/01
JO  - Neuron
DO  - 10.1016/j.neuron.2026.08.007
UR  - https://doi.org/10.1016/j.neuron.2026.08.007
AB  - How cell-type-specific nucleus accumbens (NAc) circuits encode social interactions, and whether this encoding is disrupted in autism spectrum disorder (ASD), remains unresolved. Using longitudinal miniscope calcium imaging and optogenetics in mice, we show that NAc core population activity selectively encodes social interaction and that NAc inhibition enhances sociability. In Cntnap2 −/− mice, both acute and cross-day social representations are degraded, and NAc inhibition persistently improves sociability. Cell-type-specific recordings and optogenetics reveal opposing medium spiny neuron (MSN) contributions: D1-MSNs promote sociability, and D2-MSNs suppress it. Cntnap2 −/− mice exhibit selective depletion of socially excited D1-MSNs and socially inhibited D2-MSNs, along with impaired cross-day population decoding. D2-MSN inhibition improves social behavior in Cntnap2 −/− mice, and D1-MSN activation does not. Together, these findings link disrupted, cell-type-specific NAc social representations to ASD-related social dysfunction and suggest that targeted modulation of NAc activity may improve social behavior.
SN  - 0896-6273
SN  - 1097-4199
ER  -