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PreprintCC BY-NC-NDbioRxiv

Decay chemicals activate a pH-sensing pathway to initiate a persistent state

  1. 11. Department of Neurobiology, School of Biological Sciences. University of California, San Diego. La Jolla, CA

Abstract

Animals use multiple sensory systems to identify signs of danger, including dead conspecifics. Fish can identify decaying conspecifics from chemosensory cues, which prompt a long-lasting avoidance; the neural basis of this persistent chemosensory-driven state is not understood. Here, we describe a persistent alarm state in larval zebrafish, where brief exposure to the polyamine decay product, cadaverine, initiates a minutes-long increase in heart rate and suppression of visually-evoked swimming. Cadaverine activates both olfactory and trigeminal neurons, with persistently-active cells in the forebrain and dorsolateral hindbrain. However, we find that cadaverine's persistent effects on hindbrain activity, heart rate, and locomotor suppression are not mediated by olfaction. Instead, they are mediated through trigeminal chemosensation of the basic pH of concentrated cadaverine in solution. Knockout of TrpA1 channels, which are expressed in trigeminal neurons and associated with chemical nociception across species, prevents the persistent suppression of movement from brief exposure to cadaverine. pH-responsive trigeminal neurons project into the dorsolateral hindbrain to mediate persistent activity and long-lasting locomotor suppression through local inhibition. These results demonstrate that non-olfactory chemosensation mediates persistent behavioral responses to death and decay in zebrafish, illustrating how diverse chemosensory systems detect ethologically-relevant cues to drive adaptive behavior.

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BibTeX
@misc{padilla2026decay,
  title = {{Decay chemicals activate a pH-sensing pathway to initiate a persistent state}},
  author = {G. M. Padilla and M. L. White and M. T. Ngan and J. Jefferson and J. Swindlehurst Chan and K. A. Martin and M. Lovett-Barron},
  howpublished = {bioRxiv},
  year = {2026},
  month = sep,
  doi = {10.64898/2026.09.16.751831},
  url = {https://www.biorxiv.org/content/10.64898/2026.09.16.751831v1},
  note = {CC BY-NC-ND},
}
RIS
TY  - UNPB
TI  - Decay chemicals activate a pH-sensing pathway to initiate a persistent state
AU  - G. M. Padilla
AU  - M. L. White
AU  - M. T. Ngan
AU  - J. Jefferson
AU  - J. Swindlehurst Chan
AU  - K. A. Martin
AU  - M. Lovett-Barron
PY  - 2026
DA  - 2026/09/16
PB  - bioRxiv
DO  - 10.64898/2026.09.16.751831
UR  - https://www.biorxiv.org/content/10.64898/2026.09.16.751831v1
AB  - Animals use multiple sensory systems to identify signs of danger, including dead conspecifics. Fish can identify decaying conspecifics from chemosensory cues, which prompt a long-lasting avoidance; the neural basis of this persistent chemosensory-driven state is not understood. Here, we describe a persistent alarm state in larval zebrafish, where brief exposure to the polyamine decay product, cadaverine, initiates a minutes-long increase in heart rate and suppression of visually-evoked swimming. Cadaverine activates both olfactory and trigeminal neurons, with persistently-active cells in the forebrain and dorsolateral hindbrain. However, we find that cadaverine's persistent effects on hindbrain activity, heart rate, and locomotor suppression are not mediated by olfaction. Instead, they are mediated through trigeminal chemosensation of the basic pH of concentrated cadaverine in solution. Knockout of TrpA1 channels, which are expressed in trigeminal neurons and associated with chemical nociception across species, prevents the persistent suppression of movement from brief exposure to cadaverine. pH-responsive trigeminal neurons project into the dorsolateral hindbrain to mediate persistent activity and long-lasting locomotor suppression through local inhibition. These results demonstrate that non-olfactory chemosensation mediates persistent behavioral responses to death and decay in zebrafish, illustrating how diverse chemosensory systems detect ethologically-relevant cues to drive adaptive behavior.
ER  -