Coding of chromatic spatial contrast by macaque V1 neurons

  1. Abhishek De
  2. Gregory D Horwitz  Is a corresponding author
  1. University of Washington, United States


Color perception relies on comparisons between adjacent lights, but how the brain performs these comparisons is poorly understood. To elucidate the underlying neural mechanisms, we recorded spiking responses of individual V1 neurons in macaque monkeys to pairs of stimuli within the classical receptive field (RF). We estimated the spatial-chromatic RF of each neuron and then presented customized colored edges using a novel closed-loop technique. We found that many double-opponent (DO) cells, which have spatially and chromatically opponent RFs, responded to chromatic contrast as a weighted sum, akin to how other V1 cells responded to luminance contrast. Yet other neurons integrated chromatic signals non-linearly, confirming that linear signal integration is not an obligate property of V1 neurons. The functional similarity of cone-opponent DO cells and cone non-opponent simple cells suggests that these two groups may share a common underlying neural circuitry, promotes the construction of image-computable models for full-color image representation, and sheds new light on V1 complex cells.

Data availability

All data associated with this study are available at

The following data sets were generated

Article and author information

Author details

  1. Abhishek De

    Department of Physiology and Biophysics, University of Washington, Seattle, United States
    Competing interests
    The authors declare that no competing interests exist.
    ORCID icon "This ORCID iD identifies the author of this article:" 0000-0002-2978-473X
  2. Gregory D Horwitz

    Department of Physiology and Biophysics, University of Washington, Seattle, 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:" 0000-0001-5130-5259


National Eye Institute (EY018849)

  • Gregory D Horwitz

Office of the Director (OD010425)

  • Gregory D Horwitz

National Eye Institute (EY01730)

  • Gregory D Horwitz

National Institute on Drug Abuse (DA033461)

  • Abhishek De

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


Animal experimentation: This study was performed in strict accordance with the recommendations in the Guide for the Care and Use of Laboratory Animals of the National Institutes of Health. All of the animals were handled according to approved institutional animal care and use committee (IACUC) protocol (#4167-01) of the University of Washington. All surgery was performed under sevoflurane anesthesia, and every effort was made to minimize suffering.

Reviewing Editor

  1. Tatiana Pasternak, National Institute of Neurological Disorders and Stroke, United States

Publication history

  1. Preprint posted: February 14, 2021 (view preprint)
  2. Received: March 5, 2021
  3. Accepted: February 1, 2022
  4. Accepted Manuscript published: February 11, 2022 (version 1)
  5. Version of Record published: March 14, 2022 (version 2)


© 2022, De & Horwitz

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.


  • 632
    Page views
  • 79
  • 0

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

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. Abhishek De
  2. Gregory D Horwitz
Coding of chromatic spatial contrast by macaque V1 neurons
eLife 11:e68133.

Further reading

    1. Cell Biology
    2. Neuroscience
    Arnau Llobet Rosell, Maria Paglione ... Lukas Jakob Neukomm
    Research Article

    Axon degeneration contributes to the disruption of neuronal circuit function in diseased and injured nervous systems. Severed axons degenerate following the activation of an evolutionarily conserved signaling pathway, which culminates in the activation of SARM1 in mammals to execute the pathological depletion of the metabolite NAD+. SARM1 NADase activity is activated by the NAD+ precursor nicotinamide mononucleotide (NMN). In mammals, keeping NMN levels low potently preserves axons after injury. However, it remains unclear whether NMN is also a key mediator of axon degeneration and dSarm activation in flies. Here, we demonstrate that lowering NMN levels in Drosophila through the expression of a newly generated prokaryotic NMN-Deamidase (NMN-D) preserves severed axons for months and keeps them circuit-integrated for weeks. NMN-D alters the NAD+ metabolic flux by lowering NMN, while NAD+ remains unchanged in vivo. Increased NMN synthesis, by the expression of mouse nicotinamide phosphoribosyltransferase (mNAMPT), leads to faster axon degeneration after injury. We also show that NMN-induced activation of dSarm mediates axon degeneration in vivo. Finally, NMN-D delays neurodegeneration caused by loss of the sole NMN-consuming and NAD+-synthesizing enzyme dNmnat. Our results reveal a critical role for NMN in neurodegeneration in the fly, which extends beyond axonal injury. The potent neuroprotection by reducing NMN levels is similar to the interference with other essential mediators of axon degeneration in Drosophila.

    1. Neuroscience
    Kasra Manoocheri, Adam G Carter
    Research Article

    Connections from the basolateral amygdala (BLA) to medial prefrontal cortex (PFC) regulate memory and emotion and become disrupted in neuropsychiatric disorders. The diverse roles attributed to interactions between the BLA and PFC may reflect multiple circuits nested within a wider network. To examine these circuits, we first used retrograde and anterograde anatomy to show that the rostral BLA (rBLA) and caudal BLA (cBLA) differentially project to prelimbic (PL) and infralimbic (IL) subregions of the mouse PFC. Using ex vivo whole-cell recordings and optogenetics, we then assessed which neuronal subtypes are targeted, showing that rBLA preferentially drives layer 2 (L2) cortico-amygdalar (CA) neurons in PL, whereas cBLA drives layer 5 (L5) pyramidal tract (PT) neurons in IL. We next combined in vivo silicon probe recordings and optogenetics to confirm that cBLA mainly influences IL L5, whereas rBLA primarily activates PL L2, but also evokes polysynaptic activity in PL L5. Lastly, we used soma-tagged optogenetics to explore the local circuits linking superficial and deep layers of PL, showing how rBLA can engage L2 CA neurons to impact L5 PT neuron activity. Together, our findings delineate how subregions of the BLA target distinct networks within the PFC and differentially influence output from PL and IL.