Abstract

Both adult and larval zebrafish have been demonstrated to show behavioural responses to noxious stimulation but also to potentially stress- and fear or anxiety- eliciting situations. The pain or nociceptive response can be altered and modulated by these situations in adult fish through a mechanism called stress-induced analgesia. However, this phenomenon has not been described in larval fish yet. Therefore, this study explores the behavioural changes in larval zebrafish after noxious stimulation and exposure to challenges that can trigger a stress, fear or anxiety reaction. Five-day post fertilization zebrafish were exposed to either a stressor (air emersion), a predatory fear cue (alarm substance) or an anxiogenic (caffeine) alone or prior to immersion in acetic acid 0.1%. Pre- and post-stimulation behaviour (swimming velocity and time spent active) was recorded using a novel tracking software in 25 fish at once. Results show that larvae reduced both velocity and activity after exposure to the air emersion and alarm substance challenges and that these changes were attenuated using etomidate and diazepam, respectively. Exposure to acetic acid decreased velocity and activity as well, whereas air emersion and alarm substance inhibited these responses, showing no differences between pre- and post-stimulation. Therefore, we hypothesize that an antinociceptive mechanism, activated by stress and/or fear, occur in 5dpf zebrafish, which could have prevented the larvae to display the characteristic responses to pain.

Highlights

  • Nociception is the sensory mechanism used to perceive actual or potential tissue damage

  • Air emersion followed by exposure to acetic acid 0.1% did not influence swimming velocity or time spent active from pre-treatment values (Figs 2 and 3)

  • Our results show that the behavioural responses observed in the group exposed to a potentially noxious stimulus, i.e. immersion in acetic acid 0.1%, is inhibited by previous exposure to either air emersion and alarm substance

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Summary

Introduction

Nociception is the sensory mechanism used to perceive actual or potential tissue damage. The neurons that mediate nociceptive information are called nociceptors. Fish can perceive and respond to a wide range of stimuli, including mechanical [1], thermal [2], electrical [3] or chemical [4]. Recent investigations have reported the presence of these neurons in fish [1,5], which, along with the findings of nociceptive pathways and brain activity [6,7] and the regulation of novel candidate genes after a nociceptive event [8], suggest that fish are capable of nociception. Changes in the behaviour have been recorded after exposure to noxious stimulation [9,10,11] and these have been ameliorated by administering analgesia [5].

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