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Distinct relationships of parietal and prefrontal cortices to evidence accumulation

Nature volume 520, pages 220223 (09 April 2015) | Download Citation


Gradual accumulation of evidence is thought to be fundamental for decision-making, and its neural correlates have been found in several brain regions1,2,3,4,5,6,7,8. Here we develop a generalizable method to measure tuning curves that specify the relationship between neural responses and mentally accumulated evidence, and apply it to distinguish the encoding of decision variables in posterior parietal cortex and prefrontal cortex (frontal orienting fields, FOF). We recorded the firing rates of neurons in posterior parietal cortex and FOF from rats performing a perceptual decision-making task. Classical analyses uncovered correlates of accumulating evidence, similar to previous observations in primates and also similar across the two regions. However, tuning curve assays revealed that while the posterior parietal cortex encodes a graded value of the accumulating evidence, the FOF has a more categorical encoding that indicates, throughout the trial, the decision provisionally favoured by the evidence accumulated so far. Contrary to current views3,5,7,8,9, this suggests that premotor activity in the frontal cortex does not have a role in the accumulation process, but instead has a more categorical function, such as transforming accumulated evidence into a discrete choice. To probe causally the role of FOF activity, we optogenetically silenced it during different time points of the trial. Consistent with a role in committing to a categorical choice at the end of the evidence accumulation process, but not consistent with a role during the accumulation itself, a behavioural effect was observed only when FOF silencing occurred at the end of the perceptual stimulus. Our results place important constraints on the circuit logic of brain regions involved in decision-making.

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We thank K. Deisseroth for support with optogenetics. We thank A. Akrami, T. Buschman, J. Gold, B. Pesaran, B. Scott, D. Tank and M. Yartsev for comments on the manuscript. We thank A. Begelfer, K. Osorio and J. Teran for animal and laboratory support. T.D.H. was supported by National Institutes of Health (NIH) Award Number F32MH098572. C.A.D. was supported by a Howard Hughes Medical Institute predoctoral fellowship. C.D.K. was supported in part by the NIH Award Number T32MH065214.

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Author notes

    • Timothy D. Hanks
    •  & Charles D. Kopec

    These authors contributed equally to this work.


  1. Princeton Neuroscience Institute, Princeton University, Princeton, New Jersey 08544, USA

    • Timothy D. Hanks
    • , Charles D. Kopec
    • , Bingni W. Brunton
    • , Chunyu A. Duan
    • , Jeffrey C. Erlich
    •  & Carlos D. Brody
  2. Department of Molecular Biology, Princeton University, Princeton, New Jersey 08544, USA

    • Timothy D. Hanks
    • , Charles D. Kopec
    • , Bingni W. Brunton
    • , Chunyu A. Duan
    • , Jeffrey C. Erlich
    •  & Carlos D. Brody
  3. Departments of Biology and Applied Mathematics, University of Washington, Seattle, Washington 98105, USA

    • Bingni W. Brunton
  4. NYU-ECNU Institute of Brain and Cognitive Science, NYU-Shanghai, Shanghai 200122, China

    • Jeffrey C. Erlich
  5. Howard Hughes Medical Institute, Princeton University, Princeton, New Jersey 08544, USA

    • Carlos D. Brody


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T.D.H., B.W.B., C.A.D. and J.C.E. collected electrophysiological data. T.D.H. analysed electrophysiological data. J.C.E. played an advisory role on electrophysiological experiments. C.D.K. carried out the optogenetic experiments, with assistance from B.W.B. C.D.K. analysed the optogenetics data, with input and assistance from T.D.H. and J.C.E. T.D.H., C.D.K. and C.D.B. wrote the paper. C.D.B. was involved in all aspects of experimental design and data analysis.

Competing interests

The authors declare no competing financial interests.

Corresponding author

Correspondence to Carlos D. Brody.

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