PUBLICATION
Catecholamines modulate the hypoxic ventilatory response of larval zebrafish (Danio rerio)
- Authors
- Pan, Y.K., Julian, T., Garvey, K., Perry, S.F.
- ID
- ZDB-PUB-221210-4
- Date
- 2022
- Source
- The Journal of experimental biology 226(1): (Journal)
- Registered Authors
- Perry, Steve F.
- Keywords
- Adrenaline, Beta-adrenoreceptor, Catecholamines, Hypoxia, Hypoxic ventilatory response, Knockout
- MeSH Terms
-
- Animals
- Catecholamines*/metabolism
- Epinephrine/pharmacology
- Hypoxia
- Larva/metabolism
- Propranolol/metabolism
- Receptors, Adrenergic, beta/metabolism
- Zebrafish*/physiology
- PubMed
- 36484145 Full text @ J. Exp. Biol.
Citation
Pan, Y.K., Julian, T., Garvey, K., Perry, S.F. (2022) Catecholamines modulate the hypoxic ventilatory response of larval zebrafish (Danio rerio). The Journal of experimental biology. 226(1):.
Abstract
The hypoxic ventilatory response (HVR) in fish is an important reflex that aids O2 uptake when low environmental O2 levels constrain diffusion. In developing zebrafish (Danio rerio), the acute HVR is multiphasic, consisting of a rapid increase in ventilation frequency (fV) during hypoxia onset, followed by a decline to a stable plateau phase above fV under normoxic conditions. In this study, we examined the potential role of catecholamines in contributing to each of these phases of the dynamic HVR in zebrafish larvae. We showed that adrenaline elicits a dose-dependent β-adrenoreceptor (AR)-mediated increase in fV that does not require expression of β1-ARs, as the hyperventilatory response to β-AR stimulation was unaltered in adrb1-/- mutants, generated by CRISPR/Cas9 knockout. In response to hypoxia and propranolol co-treatment, the magnitude of the rapidly occurring peak increase in fV during hypoxia onset was attenuated (112±14 breaths min-1 without propranolol to 68±17 breaths min-1 with propranolol), whereas the increased fV during the stable phase of the HVR was prevented in both wild-types and adrb1-/- mutants. Thus β1-AR is not required for the HVR, and other β-ARs, though not required for the initiation of the HVR, are involved in setting the maximal increase in fV and in maintaining hyperventilation during continued hypoxia. This adrenergic modulation of the HVR may arise from centrally released catecholamines because adrenaline exposure failed to activate (based on intracellular Ca2+ levels) cranial nerves IX and X, which transmit O2 signals from the pharyngeal arch to the central nervous system.
Genes / Markers
Expression
Phenotype
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Fish
Orthology
Engineered Foreign Genes
Mapping