ZFIN ID: ZDB-PUB-120927-13
Cortisol regulates Na(+) uptake in zebrafish, Danio rerio, larvae via the glucocorticoid receptor
Kumai, Y., Nesan, D., Vijayan, M.M., and Perry, S.F.
Date: 2012
Source: Molecular and Cellular Endocrinology   364(1-2): 113-125 (Journal)
Registered Authors: Perry, Steve F.
Keywords: cortisol, glucocorticoid receptor, zebrafish, Rhcg1, Na+-H+ exchanger 3b, low ph
MeSH Terms:
  • Acclimatization
  • Aldosterone/pharmacology
  • Ammonia/pharmacology
  • Animals
  • Anti-Inflammatory Agents/pharmacology*
  • Cation Transport Proteins/antagonists & inhibitors
  • Cation Transport Proteins/metabolism*
  • Dexamethasone/pharmacology
  • Hormone Antagonists/pharmacology
  • Hydrocortisone/pharmacology*
  • Hydrogen-Ion Concentration
  • Ion Transport/drug effects
  • Larva/drug effects
  • Larva/physiology
  • Mifepristone/pharmacology
  • RNA, Small Interfering/genetics
  • Receptors, Glucocorticoid/agonists
  • Receptors, Glucocorticoid/antagonists & inhibitors
  • Receptors, Glucocorticoid/metabolism*
  • Receptors, Mineralocorticoid/agonists
  • Receptors, Mineralocorticoid/metabolism
  • Sodium/metabolism*
  • Sodium-Hydrogen Exchangers/antagonists & inhibitors
  • Sodium-Hydrogen Exchangers/metabolism*
  • Zebrafish/physiology*
  • Zebrafish Proteins/antagonists & inhibitors
  • Zebrafish Proteins/metabolism*
PubMed: 22963886 Full text @ Mol. Cell. Endocrinol.
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ABSTRACT

Unlike other freshwater fish previously examined, zebrafish are capable of increasing their rate of Na+ uptake during chronic exposure to acidic water (pH 4). In the present study, the potential role of cortisol in the induction of Na+ uptake during acid-exposure was investigated. When zebrafish larvae (4 days post-fertilization) were treated with waterborne cortisol, the rate of Na+ uptake was significantly increased; this effect was blocked by co-incubating larvae with RU-486, an antagonist selective for the glucocorticoid receptor (GR). A similar induction in Na+ uptake, which was also blocked by RU-486, was observed when larvae were treated with dexamethasone, a selective GR agonist. Conversely, treating larvae with aldosterone, a selective agonist for the mineralocorticoid receptor (MR) had no effect on Na+ uptake. Acid-exposure increased whole body cortisol levels and translational knockdown of GR using antisense morpholinos prevented the full induction of Na+ uptake during exposure to acidic water, further confirming the role of cortisol and GR in Na+ uptake stimulation. Using immunohistochemistry, GR was localized to ionocytes known to be responsible for Na+ uptake (HR-cells). Knockdown of Rhcg1, an apical membrane ammonia channel or Na+/H+ exchanger 3b (NHE3b), proteins known to play an important role in facilitating Na+ uptake in acidic water, prevented the stimulatory effects of cortisol treatment on Na+ uptake, suggesting that cortisol regulates Na+ uptake by stimulating an Rhcg1–NHE3b “functional metabolon”.

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