1. Neuroscience
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When complex neuronal structures may not matter

  1. Adriane G Otopalik  Is a corresponding author
  2. Alexander C Sutton
  3. Matthew Ryan Banghart
  4. Eve Marder  Is a corresponding author
  1. Brandeis University, United States
  2. Harvard Medical School, United States
Research Article
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Cite this article as: eLife 2017;6:e23508 doi: 10.7554/eLife.23508


Much work has explored animal-to-animal variability and compensation in ion channel expression. Yet, little is known regarding the physiological consequences of morphological variability. We quantify animal-to-animal variability in cable lengths (CV = 0.4) and branching patterns in the Gastric Mill (GM) neuron, an identified neuron type with highly-conserved physiological properties in the crustacean stomatogastric ganglion (STG) of Cancer borealis. We examined passive GM electrotonic structure by measuring the amplitudes and apparent reversal potentials (Erevs) of inhibitory responses evoked with focal glutamate photo-uncaging in the presence of TTX. Apparent Erevs were relatively invariant across sites (mean CV + SD =0.04 + 0.01; 7-20 sites in each of 10 neurons), which ranged between 100-800 µm from the somatic recording site. Thus, GM neurons are remarkably electrotonically compact (estimated λ > 1.5 mm). Electrotonically compact structures, in consort with graded transmission, provide an elegant solution to observed morphological variability in the STG.

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Author details

  1. Adriane G Otopalik

    Volen Center, Brandeis University, Waltham, United States
    For correspondence
    Competing interests
    No competing interests declared.
    ORCID icon "This ORCID iD identifies the author of this article:" 0000-0002-3224-6502
  2. Alexander C Sutton

    Volen Center, Brandeis University, Waltham, United States
    Competing interests
    No competing interests declared.
  3. Matthew Ryan Banghart

    Department of Neurobiology, Harvard Medical School, Boston, United States
    Competing interests
    No competing interests declared.
  4. Eve Marder

    Volen Center, Brandeis University, Waltham, United States
    For correspondence
    Competing interests
    Eve Marder, Senior editor, eLife.
    ORCID icon "This ORCID iD identifies the author of this article:" 0000-0001-9632-5448


National Institute of Neurological Disorders and Stroke (F31NS092126)

  • Adriane G Otopalik

National Institute of Neurological Disorders and Stroke (R37NS017813)

  • Eve Marder

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

Reviewing Editor

  1. Indira M Raman, Northwestern University, United States

Publication history

  1. Received: November 21, 2016
  2. Accepted: February 6, 2017
  3. Accepted Manuscript published: February 6, 2017 (version 1)
  4. Version of Record published: February 23, 2017 (version 2)


© 2017, Otopalik et al.

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.


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Further reading

    1. Neuroscience
    Adriane G Otopalik et al.
    Research Article Updated

    Neuronal physiology depends on a neuron’s ion channel composition and unique morphology. Variable ion channel compositions can produce similar neuronal physiologies across animals. Less is known regarding the morphological precision required to produce reliable neuronal physiology. Theoretical studies suggest that moraphology is tightly tuned to minimize wiring and conduction delay of synaptic events. We utilize high-resolution confocal microscopy and custom computational tools to characterize the morphologies of four neuron types in the stomatogastric ganglion (STG) of the crab Cancer borealis. Macroscopic branching patterns and fine cable properties are variable within and across neuron types. We compare these neuronal structures to synthetic minimal spanning neurite trees constrained by a wiring cost equation and find that STG neurons do not adhere to prevailing hypotheses regarding wiring optimization principles. In this highly modulated and oscillating circuit, neuronal structures appear to be governed by a space-filling mechanism that outweighs the cost of inefficient wiring.

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    Research Article Updated

    Prion diseases are caused by PrPSc, a self-replicating pathologically misfolded protein that exerts toxicity predominantly in the brain. The administration of PrPSc causes a robust, reproducible and specific disease manifestation. Here, we have applied a combination of translating ribosome affinity purification and ribosome profiling to identify biologically relevant prion-induced changes during disease progression in a cell-type-specific and genome-wide manner. Terminally diseased mice with severe neurological symptoms showed extensive alterations in astrocytes and microglia. Surprisingly, we detected only minor changes in the translational profiles of neurons. Prion-induced alterations in glia overlapped with those identified in other neurodegenerative diseases, suggesting that similar events occur in a broad spectrum of pathologies. Our results suggest that aberrant translation within glia may suffice to cause severe neurological symptoms and may even be the primary driver of prion disease.