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Publication Detail
Cellular basis of transduction in carotid chemoreceptors.
  • Publication Type:
    Journal article
  • Publication Sub Type:
    Journal Article
  • Authors:
    Biscoe TJ, Duchen MR
  • Publication date:
    06/1990
  • Pagination:
    L271, L278
  • Journal:
    Am J Physiol
  • Volume:
    258
  • Issue:
    6 Pt 1
  • Status:
    Published
  • Country:
    United States
  • Print ISSN:
    0002-9513
  • Language:
    eng
  • Keywords:
    Animals, Calcium, Carotid Arteries, Carotid Body, Chemoreceptor Cells, Electrophysiology, Oxygen, Signal Transduction
Abstract
Understanding transduction mechanisms is central to much of sensory physiology. The carotid chemoreceptors monitor the PO2 of arterial blood en route to the brain and are powerfully excited when the arterial PO2 falls to less than 60 mmHg. The type I cell is generally believed to be the transducer. These cells release catecholamines in response to agents that excite the receptor (hypoxia, cyanide, K(+)-induced depolarization, etc.). Adherent to the cells are the saucer-shaped nerve endings of the axons of the sinus nerve. We and others have used patch-clamp techniques to study the electrophysiological properties of the type I cells. We have also investigated type I cell chemistry with microfluorometric techniques, to measure intracellular Ca2+ concentration ([Ca2+]i), mitochondrial NADH, and mitochondrial membrane potential (delta psi m). During hypoxia there are graded increases in NADH, [Ca2+]i (which presumably will promote transmitter release), and graded depolarization of delta psi m. These results suggest that the Ca2+ is largely derived from an intracellular store, probably from mitochondria, and that release is entrained to delta psi m. Comparative studies with other cells indicate an increased sensitivity of the mitochondria of type I cells to changes in PO2. The data suggest that the electrophysiological responses of type I cells to hypoxia are not central to the response, although the excitability of the cells may provide a mechanism for the modulation of the response by varying voltage-gated Ca2+ influx.
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