Presenting Author: Jodi Thomas
Authors: Jodi T. Thomas , Blake L. Spady , Philip L. Munday , Sue-Ann Watson [1,3]
1. ARC Centre of Excellence for Coral Reef Studies, James Cook University, Townsville, Queensland, Australia;
2. College of Science and Engineering, James Cook University, Townsville, Queensland, Australia;
3. Biodiversity and Geoscience Program, Museum of Tropical Queensland, Queensland Museum, Townsville, Queensland, Australia
Projected future carbon dioxide (CO2) levels in the ocean can alter the behaviour of marine animals.
Disrupted functioning of the γ – aminobutyric acid type A (GABA – A) receptor is suggested to underlie CO2 – induced behavioural changes in fish, however, the mechanisms underlying behavioural changes of marine invertebrates at elevated CO2 levels are not well understood. Here, we aimed to assess the role of GABA – A – like and other chloride (Cl – ) channel receptors in behavioural alterations at elevated CO2 in a cephalopod. We exposed two – toned py gmy squid Idiosepius pygmaeus to ambient (~450 μatm) or elevated (~1,000 μatm) CO2 levels for seven days. Squid were treated with sham, gabazine (GABA – A receptor antagonist) or picrotoxin (Cl – channel blocker) immediately before measurement of conspecific – directed behaviours and activity levels upon mirror exposure. If disrupted function of GABA – A – like and/or other Cl – channel receptors underlies the behavioural changes, we predicted that gabazine and picrotoxin would attenuate the behavioural changes at elevated CO2. Elevated CO2 increased squid activity levels and altered some, but had no meaningful effect on other, conspecific – directed behaviours. Gabazine and picrotoxin attenuated some of the behavioural changes at elevated CO2, indicating altered GABA – A – like and Cl – channel receptor functioning may underlie these behavioural changes. However, gabazine and picrotoxin had the same effect at both CO2 levels on other behavioural traits, suggesting altered function of GABA – A – like and Cl – channel receptors was not responsible for other behavioural changes at elevated CO2.
Our results suggest multiple mechanisms may be involved, which could explain variability in the effects of CO2 and drug treatment across behaviours.
No comments available