A service of Penn’s Neuroscience Graduate Group


Understanding how a few neurons in a tiny worm control eating under multiple conditions

or, technically,
Neural and genetic degeneracy underlies Caenorhabditis elegans feeding behavior. [See the original abstract on PubMed]


Authors: Nick F. Trojanowski, Olivia Padovan-Merhar, David M. Raizen, Chris Fang-Yen

Brief prepared by: Nick Trojanowski
Brief approved by: Alyse Thomas
Section Chief: Chris Palmer
Date posted: May 3, 2016
Brief in Brief (TL;DR)

What do we know: Only a few neurons control worm eating behavior. Even when you destroy most of them, the system still works properly.

What don’t we know: The purpose and function of these neurons, since the system seems to work fine without most of them.

What this study shows: Many of these neurons are capable of making the worm eat under some but not all conditions, ensuring that eating continues even when some parts of the system are changed.

What we can do in the future because of this study: We can better understand how the worm decides which neurons to use during different conditions to ensure organism survival.

Why you should care: We don’t really understand what causes most mental illnesses, but we think it has to do with systems of neurons malfunctioning. If we understand how a worm keeps working even when some parts of the nervous system break, we can better understand how to fix people’s brains when things go wrong during mental illness.

Brief for Non-Neuroscientists

For animals to survive and reproduce, it’s very important that they are able to ingest food. A microscopic worm, one that’s been studied by neuroscientists for 40 years, has a small system of neurons that controls feeding. When you individually destroy most of these neurons, the worm still eats properly. We wanted to define the purpose of the neurons that don’t seem to be critical for eating. To do this, we used a technique called optogenetics, which allows us to turn on neurons by shining a blue light on them. By turning on the neurons one by one, we found that many of the individual neurons initiate eating behavior. This result explains why previous studies found no change in eating after destroying individual neurons: some neurons can do the same job as other neurons, depending on the conditions. We also found that under certain conditions, destroying some of these neurons did affect eating, so these neurons don’t always have exactly the same functions. Understanding how systems of neurons in this small worm have evolved to maintain function when some neurons are destroyed will help researchers understand how systems of neurons in other animals, such as humans, respond to changes or injuries. We hope that this will eventually allow us to understand how neurons controlling behaviors associated with mental illness go wrong and why.

Brief for Neuroscientists

Degenerate networks, in which structurally distinct elements can perform the same function or yield the same output, are ubiquitous in biology and likely provide systems the ability to ensure organism survival under various conditions. Degeneracy contributes to the robustness and adaptability of networks in varied environmental and evolutionary contexts. However, how degenerate neural networks regulate behavior in vivo is poorly understood, especially at the genetic level. Here, we identify degenerate neural and genetic mechanisms that underlie excitation of the pharynx (feeding organ) in the nematode Caenorhabditis elegans using cell-specific optogenetic excitation and inhibition. We show that the pharyngeal neurons MC, M2, M4, and I1 form multiple direct and indirect excitatory pathways in a robust network for control of pharyngeal pumping. I1 excites pumping via MC and M2 in a state-dependent manner. We identify nicotinic and muscarinic receptors through which the pharyngeal network regulates feeding rate. These results identify two different mechanisms by which degeneracy is manifest in a neural circuit in vivo.

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