PUBLICATION
Noradrenergic tone is not required for neuronal activity-induced rebound sleep in zebrafish
- Authors
- Benoit, E., Lyons, D.G., Rihel, J.
- ID
- ZDB-PUB-230723-45
- Date
- 2023
- Source
- Journal of comparative physiology. B, Biochemical, systemic, and environmental physiology 194(3): 279-298 (Journal)
- Registered Authors
- Rihel, Jason
- Keywords
- Noradrenalin, Sleep, Sleep homeostasis, Zebrafish, c-fos
- MeSH Terms
-
- Adrenergic alpha-2 Receptor Agonists/pharmacology
- Animals
- Clonidine/pharmacology
- Dopamine beta-Hydroxylase*/genetics
- Dopamine beta-Hydroxylase*/metabolism
- Larva/drug effects
- Larva/physiology
- Neurons/drug effects
- Neurons/metabolism
- Norepinephrine*/metabolism
- Proto-Oncogene Proteins c-fos/genetics
- Proto-Oncogene Proteins c-fos/metabolism
- Sleep*/drug effects
- Sleep*/physiology
- Wakefulness/drug effects
- Wakefulness/physiology
- Zebrafish*/physiology
- Zebrafish Proteins/genetics
- Zebrafish Proteins/metabolism
- PubMed
- 37480493 Full text @ J. Comp. Physiol. B
Citation
Benoit, E., Lyons, D.G., Rihel, J. (2023) Noradrenergic tone is not required for neuronal activity-induced rebound sleep in zebrafish. Journal of comparative physiology. B, Biochemical, systemic, and environmental physiology. 194(3):279-298.
Abstract
Sleep pressure builds during wakefulness, but the mechanisms underlying this homeostatic process are poorly understood. One zebrafish model suggests that sleep pressure increases as a function of global neuronal activity, such as during sleep deprivation or acute exposure to drugs that induce widespread brain activation. Given that the arousal-promoting noradrenergic system is important for maintaining heightened neuronal activity during wakefulness, we hypothesised that genetic and pharmacological reduction of noradrenergic tone during drug-induced neuronal activation would dampen subsequent rebound sleep in zebrafish larvae. During stimulant drug treatment, dampening noradrenergic tone with the α2-adrenoceptor agonist clonidine unexpectedly enhanced subsequent rebound sleep, whereas enhancing noradrenergic signalling with a cocktail of α1- and β-adrenoceptor agonists did not enhance rebound sleep. Similarly, CRISPR/Cas9-mediated elimination of the dopamine β-hydroxylase (dbh) gene, which encodes an enzyme required for noradrenalin synthesis, enhanced baseline sleep in larvae but did not prevent additional rebound sleep following acute induction of neuronal activity. Across all drug conditions, c-fos expression immediately after drug exposure correlated strongly with the amount of induced rebound sleep, but was inversely related to the strength of noradrenergic modulatory tone. These results are consistent with a model in which increases in neuronal activity, as reflected by brain-wide levels of c-fos induction, drive a sleep pressure signal that promotes rebound sleep independently of noradrenergic tone.
Genes / Markers
Expression
Phenotype
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Fish
Orthology
Engineered Foreign Genes
Mapping