Abstract
We review recent advances in the characterization of the β-adrenoceptor (AR) system of the trout and present new data on the mechanisms of β-AR desensitization. Phosphorylation of specific amino acids located in the third intracellular loop and cytoplasmic tail regions triggers β-AR desensitization. Analysis of trout β-AR sequences reveals a difference in putative phosphorylation profiles between β-AR subtypes, this suggests that each subtype (β2-, β3a- and β3b-AR) possesses different sensitivity to desensitization. β-Adrenoceptor kinase (βARK) and β-arrestin play a pivotal role in β-AR desensitization. The tissue distribution of β-arrestin and βARK mRNA in trout is reported for the first time and interestingly, both genes appear to be highly expressed in the trout red blood cell. Previous studies reported loss of β-AR binding sites in trout red blood cells following prolonged receptor activation. Reduction of β-AR mRNA levels is reported to contribute to down-regulation of β-ARs in some species. However, we did not detect a significant change in β-AR mRNA levels in trout subjected to environmental hypoxia, clenbuterol (a β-agonist) administration, or cortisol administration; therefore, changes in mRNA levels may not contribute to β-AR desensitization in trout.
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Nickerson, J., Drouin, G., Perry, S. et al. In vitro Regulation of β-adrenoceptor Signaling in the Rainbow Trout, Oncorhynchus mykiss . Fish Physiology and Biochemistry 27, 157–171 (2002). https://doi.org/10.1023/B:FISH.0000032723.78349.4e
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DOI: https://doi.org/10.1023/B:FISH.0000032723.78349.4e
- beta-arrestin
- beta-receptor kinase
- clenbuterol
- cortisol
- down-regulation
- hypoxia
- phosphorylation