Neural basis of compositional control

Nature作者:Assia Chericoni2026年8月12日正文已收录本站

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Acknowledgements

We thank P. Schrater, X. Pitkow, J. Pearson, S. Linderman, H. Ritz and A. Shenhav for invaluable discussions and insights on solving the controller problems; J. Johnston for discussion on neural analysis; J. Adkinson, R. Mathura and V. Pirtle for invaluable assistance; and A. Thome for early and visionary efforts in developing this task and core questions.

Funding

This project was supported by NIH grants R01 DA038615, R01 MH125377, U01 NS121472, and R01 MH129439, and by the McNair foundation.

Author information

Author notes

  1. These authors contributed equally: Assia Chericoni, Justin M. Fine

  2. These authors jointly supervised this work: Sameer A. Sheth, Benjamin Y. Hayden

Authors and Affiliations

  1. Department of Neurosurgery, Baylor College of Medicine, Houston, TX, USA

    Assia Chericoni, Justin M. Fine, Taha S. Ismail, Melissa C. Franch, Elizabeth Mickiewicz, Ana G. Chavez, Eleonora Bartoli, Danika L. Paulo, Garrett P. Banks, Nisha Giridharan, Nicole R. Provenza, Andrew Watrous, Sameer A. Sheth & Benjamin Y. Hayden

  2. Department of Neuroscience, University of Minnesota, Minneapolis, MN, USA

    Gabriela Delgado Salazar

  3. Department of Electrical and Computer Engineering, Rice University, Houston, TX, USA

    Vaishnav Krishnan, Nicole R. Provenza, Sameer A. Sheth & Benjamin Y. Hayden

  4. Department of Neuroscience, Baylor College of Medicine, Houston, TX, USA

    Eleonora Bartoli, Vaishnav Krishnan, Nicole R. Provenza, Sameer A. Sheth & Benjamin Y. Hayden

  5. Department of Neurology, Baylor College of Medicine, Houston, TX, USA

    Vaishnav Krishnan, Mohamed Hegazy, Alica M. Goldman & Lu Lin

  6. Department of Psychiatry and Behavioral Sciences, Baylor College of Medicine, Houston, TX, USA

    Vaishnav Krishnan & Sameer A. Sheth

  7. Department of Neurosurgery, Michael E. DeBakey VA Medical Center, Houston, TX, USA

    Garrett P. Banks

  8. Department of Neurosurgery, College of Medicine, Imam Abdulrahman Bin Faisal University, Dammam, Saudi Arabia

    Mohammed Hasen

  9. Department of Bioengineering, Rice University, Houston, TX, USA

    Nicole R. Provenza

  10. Neuroengineering Initiative, Rice University, Houston, TX, USA

    Nicole R. Provenza, Sameer A. Sheth & Benjamin Y. Hayden

  11. Center for Neuroscience Imaging Research, Sungkyunkwan University, Suwon, South Korea

    Seng Bum Michael Yoo

  12. Department of Biomedical Engineering, Sungkyunkwan University, Suwon, South Korea

    Seng Bum Michael Yoo

  13. Department of Intelligence Health Precision Convergence, Sungkyunkwan University, Suwon, South Korea

    Seng Bum Michael Yoo

  14. Gordon and Mary Cain Pediatric Neurology Research Foundation Laboratories, Jan and Dan Duncan Neurological Research Institute, Texas Children’s Hospital, Houston, TX, USA

    Sameer A. Sheth

Authors

  1. Assia Chericoni
  2. Justin M. Fine
  3. Taha S. Ismail
  4. Gabriela Delgado Salazar
  5. Melissa C. Franch
  6. Elizabeth Mickiewicz
  7. Ana G. Chavez
  8. Eleonora Bartoli
  9. Danika L. Paulo
  10. Vaishnav Krishnan
  11. Mohamed Hegazy
  12. Alica M. Goldman
  13. Lu Lin
  14. Garrett P. Banks
  15. Nisha Giridharan
  16. Mohammed Hasen
  17. Nicole R. Provenza
  18. Andrew Watrous
  19. Seng Bum Michael Yoo
  20. Sameer A. Sheth
  21. Benjamin Y. Hayden

Contributions

J.M.F. and A.C. devised and further developed the modelling approach, respectively. J.M.F., A.C. and T.S.I. validated the modelling approach. J.M.F., A.C. and T.S.I. implemented the analysis codes. A.C., J.M.F. and B.Y.H. designed the experimental procedure and downstream analysis. D.L.P., G.P.B., N.G., M. Hasen and S.A.S. performed the intracranial stereotactic surgery. V.K., M. Hegazy, A.M.G. and L.L. provided neurological care for the study participants. J.M.F., A.C. and B.Y.H. drafted the manuscript. J.M.F. and A.C. devised and further developed the neural analyses, respectively. J.M.F., A.C. and T.S.I. implemented them. A.C., T.S.I., M.C.F., E.A.M. and A.G.C. collected the sEEG data. G.D.S., A.C. and E.A.M. collected the behavioural data. E.B., N.R.P. and A.W. contributed to data collection. E.B., N.R.P., A.W. and S.B.M.Y. contributed to data interpretation.

Corresponding author

Correspondence to Benjamin Y. Hayden.

Ethics declarations

Competing interests

S.A.S. is a consultant for Boston Scientific, Abbott, Koh Young, Neuropace, Zimmer Biomet and co-founder of Motif Neurotech. The other authors declare no competing interests.

Peer review

Peer review information

Nature thanks Sebastian Musslick and the other, anonymous, reviewers for their contribution to the peer review of this work. Peer reviewer reports are available.

Additional information

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Extended data figures and tables

Extended Data Fig. 1 Model recovery of wt value and time at switch point (wt = 0.5, t = 0 ms).

(A). Empirical simulation regime (n = 30 simulations × 30 trials × 2 prey-controllers): distribution of recovered wt values at the true switch point (wt = 0.5), quantifying bias in switch magnitude recovery across controller models. Red line indicates the median recovered value; dashed lines indicate the central 95% interval of the recovered distribution. (B). Distribution of temporal lag between recovered and true switch times for wt = 0.5, quantifying timing accuracy of switch detection across controller models. Red line indicates the median lag; dashed lines indicate the 95% CI. (C–D). Same as (A–B), but for the random 1-5 simulation regime. (E–F). Same as (A–B), but for the random 1-40 simulation regime.

Extended Data Fig. 2 Model recovery of controller gains across controller classes.

(A). Empirical simulation regime (n = 30 simulations × 30 trials × 2 prey-controllers): scatter plot showing the relationship between the simulated gains and the gains recovered from the model. Each point represents one recovered gain form a simulated trial. Each column represents a controller class. (B). Same as panel A, but for the random 1-5 simulation regime. (C). Same as panel A, but for the random 1-40 simulation regime.

Extended Data Fig. 3 Relationship between recovered controller gains and recovered wt trajectories across controller classes.

(A). Empirical simulation regime (30 simulations × 30 trials × 2 prey-specific controllers): scatter plots showing the relationship between recovered controller gains and recovered wt trajectories at the start, middle, and end of the trial. Each point represents one recovered gain estimate from one prey-specific policy in a simulated trial. Each column represents a controller class. Pearson’s correlation coefficient (r) is shown for each trial epoch. (B). Same as panel A, but for the random 1-5 simulation regime. (C). Same as panel A, but for the random 1-40 simulation regime.

Extended Data Fig. 4 Pairwise relationships between recovered controller gains across controller classes.

(A). Empirical simulation regime (30 simulations × 30 trials × 2 prey-specific controllers): scatter plots showing pairwise relationships between recovered controller gains across controller classes. Each point represents one recovered gain estimate from a simulated trial. Pearson’s correlation coefficient (r) is shown for each gain pair. (B). Same as panel A, but for the random 1-5 simulation regime. (C). Same as panel A, but for the random 1-40 simulation regime.

Extended Data Fig. 5 Model recovery of controller class and blending parameter wt.

We simulated ground-truth trajectories using known controller class (p) and known wt profiles, considering five types of wt. Simulations were generated by sampling 20 trials across sessions, with trial durations matched to the empirical distribution (approximately 0.91, 1.45, 2.83, and 4.1 s). To fix model complexity, simulations were fit using a fixed number of basis functions, rather than the model-averaging procedure used in the main text. (A). Posterior probability of recovering the true generative controller model relative to a baseline position-only controller. Across all controller classes, the true generative model was recovered above baseline (all probabilities > 0.5). Controller classes are defined in Extended Data Table 3. (B). Correlation between true and predicted position trajectories for each generative controller class, averaged across simulated trials, showing good recovery across classes (mean r = 0.83). (C–H). Example simulations showing recovery of the ground-truth blending parameter wt for each controller class. Blue lines indicate true wt, orange lines indicate recovered wt. Left panels (scaling = 1) show low-complexity trajectories, and right panels (scaling = 5) show higher-complexity trajectories. Complexity was controlled by the scale parameter of the Gaussian process used to generate wt. Across models, the mean recovery of wt was r = 0.87.

Extended Data Fig. 6 Full model recovery confusion matrix.

To assess overall model identifiability, we performed a full confusion analysis across three simulation regimes. For each generative model corresponding to a controller class (Extended Data Table 3), we simulated datasets with known parameters (30 datasets with 30 trials each), fit all candidate models to each dataset, and selected the best-fitting model using the evidence lower bound (ELBO). (A–C). Confusion matrices quantifying how reliably each generative controller class could be distinguished from the others under the (A). empirical simulation regime, (B). random 1-5, and (C). random 1-40 simulation regimes. Recoverability was significantly above chance for controller classes p, pv and pvi (binomial test, all p < 0.0001), whereas the remaining classes showed weaker identifiability. The pv model, which provided the best fit to participant behavior, was significantly recovered (43% correct; 95% CI [0.40, 0.47], p < 0.0001), but was frequently confounded with pvi and pvf. This overlap likely reflects the nested structure of the controller classes, indicating that interpretation of fitted model identities should account for partial non-identifiability between related controller families.

Extended Data Fig. 7 Behavioral predictors of target switching and average controller dynamics.

(A). Target switch GLM restricted to sEEG subjects (n = 19), showing the contribution of behavioral predictors at two time windows before the switch onset. Left: predictors computed as the mean value within the 100 ms preceding switch onset (−100 to 0 ms). Right: predictors computed as the mean value from an earlier window preceding switch onset (−400 to −300ms). Bars indicate the mean posterior effect size (percent change), and error bars indicate the 95% credible interval, as in Fig. 2h. Asterisks indicate predictors whose 95% credible interval excluded zero. (C). Averaged wt trajectory across all the participants (n = 69).

Extended Data Table 1 Experimental cohorts and participants demographics

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Extended Data Table 2 Number of recorded neurons across participants and brain regions

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Extended Data Table 3 Controller types

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Chericoni, A., Fine, J.M., Ismail, T.S. et al. Neural basis of compositional control. Nature (2026). https://doi.org/10.1038/s41586-026-10896-8

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