henhaobio
Sign in

Abstract

In various mental disorders, dysfunction of the prefrontal cortex contributes to cognitive deficits. Here we studied how the claustrum (CLA), a nucleus sharing reciprocal connections with the cortex, may participate in these cognitive impairments. We show that specific ensembles of CLA and of medial prefrontal cortex (mPFC) neurons are activated during a task requiring cognitive control such as attentional set-shifting, i.e. the ability to shift attention towards newly relevant stimulus-reward associations while disengaging from irrelevant ones. CLA neurons exert a direct excitatory input on mPFC pyramidal cells, and chemogenetic inhibition of CLA neurons suppresses the formation of specific mPFC assemblies during attentional set-shifting. Furthermore, impairing the recruitment of specific CLA assemblies through opto/chemogenetic manipulations prevents attentional set-shifting. In conclusion, we propose that the CLA controls the reorganization of mPFC ensembles to enable attentional set-shifting, emphasizing a potential role of the CLA-mPFC network in attentional dysfunctions.

Abstract summary

Claude Opus 5.5 · xhigh effort · 2 Nov 2026 · from the abstract

Claustrum neurons provide direct excitatory input to medial prefrontal cortex pyramidal cells, and inhibiting claustrum neuronal assemblies suppresses prefrontal assembly formation and prevents attentional set-shifting.

Prefrontal cortex dysfunction underlies cognitive deficits across multiple mental disorders, but the contribution of the reciprocally connected claustrum (CLA) to these impairments remains unclear. Manipulating claustrum and medial prefrontal cortex (mPFC) neuronal ensembles during attentional set-shifting shows that claustrum activity is required for prefrontal assembly formation and set-shifting behavior.

Key results

  1. ShownDistinct neuronal ensembles in both the claustrum (CLA) and medial prefrontal cortex (mPFC) activate during attentional set-shifting, with CLA neurons providing direct excitatory input onto mPFC pyramidal cells.

    Observed during an attentional set-shifting task in which subjects shift attention toward newly relevant stimulus-reward associations while disengaging from irrelevant ones (assay details and sample sizes are not stated in the abstract). · Abstract

  2. ShownChemogenetic or optogenetic disruption of CLA neurons blocks the formation of task-specific mPFC neuronal assemblies and prevents attentional set-shifting behavior.

    Chemogenetic inhibition of CLA neurons suppressed mPFC assembly formation during set-shifting, and optogenetic/chemogenetic perturbation of specific CLA assemblies abolished behavioral set-shifting. · Abstract

Methods, data and reproducibility

Activation of claustrum (CLA) and medial prefrontal cortex (mPFC) neuronal ensembles and direct excitatory CLA inputs onto mPFC pyramidal cells were examined during an attentional set-shifting task. Optogenetic and chemogenetic manipulations were used to inhibit CLA neurons or impair recruitment of specific CLA assemblies during set-shifting.

  • Claustrum and medial prefrontal cortex neuronal ensemble activity and behavioral measurements during an attentional set-shifting task
Reproducibility gaps
The abstract does not state the experimental species, sample sizes, or links to data and analysis code.
Limitations (1)
  • The abstract does not specify the model organism, sample sizes, experimental assays used to measure ensemble activation, or quantitative behavioral statistics. · noted in this summary

Read this if you investigate how cortico-claustral circuits and prefrontal neuronal assemblies regulate cognitive flexibility and attentional set-shifting.

Citations
49

Reproducibility ledger

Nobody has reported trying to reproduce this paper yet. Did you replicate an experiment or run the code? Your report saves the next lab a week.

Sign in to file a reproducibility report.