The regulatory role of GABA(A) receptor in Actinia equina nervous system and the possible effect of global ocean acidification

Global warming and connected acidification of the world ocean attract a substantial amount of research efforts, in particular in a context of their impact on behaviour and metabolism of marine organisms, such as Cnidaria. Nevertheless, mechanisms underlying Cnidarians’ neural signalling and behaviou...

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Bibliographic Details
Published in:Pflügers Archiv - European Journal of Physiology
Main Authors: Snigirov, Sergii, Sylantyev, Sergiy
Format: Text
Language:English
Published: Springer Berlin Heidelberg 2021
Subjects:
Online Access:http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8599403/
http://www.ncbi.nlm.nih.gov/pubmed/34633524
https://doi.org/10.1007/s00424-021-02628-w
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Summary:Global warming and connected acidification of the world ocean attract a substantial amount of research efforts, in particular in a context of their impact on behaviour and metabolism of marine organisms, such as Cnidaria. Nevertheless, mechanisms underlying Cnidarians’ neural signalling and behaviour and their (possible) alterations due to the world ocean acidification remain poorly understood. Here we researched for the first time modulation of GABA(A) receptors (GABA(A)Rs) in Actinia equina (Cnidaria: Anthozoa) by pH fluctuations within a range predicted by the world ocean acidification scenarios for the next 80–100 years and by selective pharmacological activation. We found that in line with earlier studies on vertebrates, both changes of pH and activation of GABA(A)Rs with a selective allosteric agonist (diazepam) modulate electrical charge transfer through GABA(A)R and the whole-cell excitability. On top of that, diazepam modifies the animal behavioural reaction on startle response. However, despite behavioural reactions displayed by living animals are controlled by GABA(A)Rs, changes of pH do not alter them significantly. Possible mechanisms underlying the species resistance to acidification impact are discussed.