ZFIN ID: ZDB-PUB-120702-16
Mechanisms and consequences of carbon dioxide sensing in fish
Perry, S.F., and Abdallah, S.
Date: 2012
Source: Respiratory Physiology & Neurobiology   184(3): 309-315 (Review)
Registered Authors: Perry, Steve F.
Keywords: neuroepithelial cell, hypercapnia, hypoxia, zebrafish, calcium, carbonic anhydrase, carbon dioxide, control of breathing
MeSH Terms:
  • Animals
  • Carbon Dioxide/metabolism*
  • Carbonic Anhydrases/metabolism
  • Fishes/physiology*
  • Gills/cytology
  • Gills/physiology*
  • Neuroepithelial Cells/cytology
  • Neuroepithelial Cells/metabolism*
PubMed: 22705499 Full text @ Respir. Physiol. Neurobiol.
ABSTRACT

Fish possess chemoreceptors able to sense increasing levels of ambient CO2 and initiate various cardiorespiratory reflexes including hyperventilation and bradycardia. These chemoreceptors are localized predominantly to the gills, are oriented to sense the external environment and typically are stimulated by changes in environmental molecular CO2 rather than H+ (although increasing H+ may be the proximate intracellular stimulus). In zebrafish, a subset of branchial neuroepithelial cells (NECs) act as bimodal sensors of CO2 and O2, similar to the Type I (glomus) cells of the mammalian carotid body. Like O2 sensing, the mechanisms underlying CO2 detection involve the inhibition of a background K+ current leading to membrane depolarization and subsequent elevation of intracellular Ca2+ levels. Carbonic anhydrase, by catalysing the hydration of CO2 to H+ and HCO3, appears to play a critical role in reducing NEC response times and increasing the magnitude of membrane depolarization accompanying hypercapnia. In larval zebrafish, CA activity is essential for the rapid development of hypercapnic bradycardia.

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