PUBLICATION

Removing a single neuron in a vertebrate brain forever abolishes an essential behavior

Authors
Hecker, A., Schulze, W., Oster, J., Richter, D.O., Schuster, S.
ID
ZDB-PUB-200512-1
Date
2020
Source
Proceedings of the National Academy of Sciences of the United States of America   117: 3254-3260 (Journal)
Registered Authors
Keywords
ablation phenotype, axon initial segment, grandmother neuron, predator–prey, startle response
MeSH Terms
  • Animals
  • Axons/physiology
  • Embryo, Nonmammalian/physiology
  • Escape Reaction/physiology*
  • Larva/physiology
  • Nervous System/growth & development*
  • Neurons/cytology*
  • Neurons/physiology*
  • Zebrafish
PubMed
32001507 Full text @ Proc. Natl. Acad. Sci. USA
Abstract
The giant Mauthner (M) cell is the largest neuron known in the vertebrate brain. It has enabled major breakthroughs in neuroscience but its ultimate function remains surprisingly unclear: An actual survival value of M cell-mediated escapes has never been supported experimentally and ablating the cell repeatedly failed to eliminate all rapid escapes, suggesting that escapes can equally well be driven by smaller neurons. Here we applied techniques to simultaneously measure escape performance and the state of the giant M axon over an extended period following ablation of its soma. We discovered that the axon survives remarkably long and remains still fully capable of driving rapid escape behavior. By unilaterally removing one of the two M axons and comparing escapes in the same individual that could or could not recruit an M axon, we show that the giant M axon is essential for rapid escapes and that its loss means that rapid escapes are also lost forever. This allowed us to directly test the survival value of the M cell-mediated escapes and to show that the absence of this giant neuron directly affects survival in encounters with a natural predator. These findings not only offer a surprising solution to an old puzzle but demonstrate that even complex brains can trust vital functions to individual neurons. Our findings suggest that mechanisms must have evolved in parallel with the unique significance of these neurons to keep their axons alive and connected.
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