Complementary codes for odor identity and intensity in olfactory cortex

  1. Kevin A Bolding
  2. Kevin M Franks  Is a corresponding author
  1. Duke University Medical School, United States


The ability to represent both stimulus identity and intensity is fundamental for perception. Using large-scale population recordings in awake mice, we find distinct coding strategies facilitate non-interfering representations of odor identity and intensity in piriform cortex. Simply knowing which neurons were activated is sufficient to accurately represent odor identity, with no additional information about identity provided by spike time or spike count. Decoding analyses indicate that cortical odor representations are not sparse. Odorant concentration had no systematic effect on spike counts, indicating that rate cannot encode intensity. Instead, odor intensity can be encoded by temporal features of the population response. We found a subpopulation of rapid, largely concentration-invariant responses was followed by another population of responses whose latencies systematically decreased at higher concentrations. Cortical inhibition transforms olfactory bulb output to sharpen these dynamics. Our data therefore reveal complementary coding strategies that can selectively represent distinct features of a stimulus.

Article and author information

Author details

  1. Kevin A Bolding

    Department of Neurobiology, Duke University Medical School, Durham, United States
    Competing interests
    The authors declare that no competing interests exist.
  2. Kevin M Franks

    Department of Neurobiology, Duke University Medical School, Durham, United States
    For correspondence
    Competing interests
    The authors declare that no competing interests exist.
    ORCID icon "This ORCID iD identifies the author of this article:" 0000-0002-6386-9518


National Institutes of Health (DC009839)

  • Kevin M Franks

National Institutes of Health (DC015525)

  • Kevin M Franks

Edward Mallinckrodt Jr. Foundation

  • Kevin M Franks

The funders had no role in study design, data collection and interpretation, or the decision to submit the work for publication.


Animal experimentation: All experimental protocols were approved by Duke University Institutional Animal Care and Use Committee according to protocols A243-12-09 and A220-15-08.

Reviewing Editor

  1. Upinder S Bhalla, National Centre for Biological Sciences, India

Version history

  1. Received: October 24, 2016
  2. Accepted: April 1, 2017
  3. Accepted Manuscript published: April 5, 2017 (version 1)
  4. Version of Record published: May 19, 2017 (version 2)


© 2017, Bolding & Franks

This article is distributed under the terms of the Creative Commons Attribution License permitting unrestricted use and redistribution provided that the original author and source are credited.


  • 6,455
    Page views
  • 1,125
  • 98

Article citation count generated by polling the highest count across the following sources: Scopus, Crossref, PubMed Central.

Download links

A two-part list of links to download the article, or parts of the article, in various formats.

Downloads (link to download the article as PDF)

Open citations (links to open the citations from this article in various online reference manager services)

Cite this article (links to download the citations from this article in formats compatible with various reference manager tools)

  1. Kevin A Bolding
  2. Kevin M Franks
Complementary codes for odor identity and intensity in olfactory cortex
eLife 6:e22630.

Further reading

    1. Neuroscience
    Anna C Geuzebroek, Hannah Craddock ... Simon P Kelly
    Research Article Updated

    Decisions about noisy stimuli are widely understood to be made by accumulating evidence up to a decision bound that can be adjusted according to task demands. However, relatively little is known about how such mechanisms operate in continuous monitoring contexts requiring intermittent target detection. Here, we examined neural decision processes underlying detection of 1 s coherence targets within continuous random dot motion, and how they are adjusted across contexts with weak, strong, or randomly mixed weak/strong targets. Our prediction was that decision bounds would be set lower when weak targets are more prevalent. Behavioural hit and false alarm rate patterns were consistent with this, and were well captured by a bound-adjustable leaky accumulator model. However, beta-band EEG signatures of motor preparation contradicted this, instead indicating lower bounds in the strong-target context. We thus tested two alternative models in which decision-bound dynamics were constrained directly by beta measurements, respectively, featuring leaky accumulation with adjustable leak, and non-leaky accumulation of evidence referenced to an adjustable sensory-level criterion. We found that the latter model best explained both behaviour and neural dynamics, highlighting novel means of decision policy regulation and the value of neurally informed modelling.

    1. Genetics and Genomics
    2. Neuroscience
    Yoshifumi Sonobe, Soojin Lee ... Paschalis Kratsios
    Research Article Updated

    A hexanucleotide repeat expansion in C9ORF72 is the most common genetic cause of amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD). A hallmark of ALS/FTD pathology is the presence of dipeptide repeat (DPR) proteins, produced from both sense GGGGCC (poly-GA, poly-GP, poly-GR) and antisense CCCCGG (poly-PR, poly-PG, poly-PA) transcripts. Translation of sense DPRs, such as poly-GA and poly-GR, depends on non-canonical (non-AUG) initiation codons. Here, we provide evidence for canonical AUG-dependent translation of two antisense DPRs, poly-PR and poly-PG. A single AUG is required for synthesis of poly-PR, one of the most toxic DPRs. Unexpectedly, we found redundancy between three AUG codons necessary for poly-PG translation. Further, the eukaryotic translation initiation factor 2D (EIF2D), which was previously implicated in sense DPR synthesis, is not required for AUG-dependent poly-PR or poly-PG translation, suggesting that distinct translation initiation factors control DPR synthesis from sense and antisense transcripts. Our findings on DPR synthesis from the C9ORF72 locus may be broadly applicable to many other nucleotide repeat expansion disorders.