Ouabain-evoked norepinephrine release from intact rat sympathetic neurons: evidence for carrier-mediated release.

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  • Author(s): Sweadner KJ
  • Source:
    The Journal of neuroscience : the official journal of the Society for Neuroscience [J Neurosci] 1985 Sep; Vol. 5 (9), pp. 2397-406.
  • Publication Type:
    Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.
  • Language:
    English
  • Additional Information
    • Source:
      Publisher: Society for Neuroscience Country of Publication: United States NLM ID: 8102140 Publication Model: Print Cited Medium: Print ISSN: 0270-6474 (Print) Linking ISSN: 02706474 NLM ISO Abbreviation: J Neurosci Subsets: MEDLINE
    • Publication Information:
      Publication: Washington, DC : Society for Neuroscience
      Original Publication: [Baltimore, Md.] : The Society, c1981-
    • Subject Terms:
      Carrier Proteins/*physiology ; Neurons/*metabolism ; Norepinephrine/*metabolism ; Ouabain/*pharmacology ; Sympathetic Nervous System/*metabolism; Animals ; Animals, Newborn/metabolism ; Calcimycin/pharmacology ; Calcium/physiology ; Neurons/enzymology ; Potassium/pharmacology ; Rats ; Rats, Inbred Strains ; Sodium/physiology ; Sodium-Potassium-Exchanging ATPase/antagonists & inhibitors ; Sympathetic Nervous System/cytology ; Sympathetic Nervous System/enzymology ; Veratridine/pharmacology
    • Abstract:
      Inhibition of the Na,K-ATPase is known to cause transmitter release from many neurons. The mechanism of [3H]norepinephrine release was examined in primary cultures of sympathetic neurons. Ouabain caused [3H]norepinephrine release at concentrations that produced 80 to 90% inhibition of Na,K-ATPase activity. The effect of ouabain was compared with the effects of high K+ and the Ca2+ ionophore A23187. [3H]Norepinephrine release elicited by depolarization with high extracellular K+ was dependent on extracellular Ca2+, was unaffected by tetrodotoxin, was potentiated by reducing extracellular Na+, and was potentiated by the norepinephrine uptake inhibitor desipramine. These are the results expected if high K+ causes release by exocytosis, and if blockade of the Na+-dependent norepinephrine uptake system increases the net measurable release of the transmitter. The Ca2+ ionophore A23187 caused [3H]norepinephrine release that was not dependent on extracellular Ca2+ but which was like the release elicited by high K+ in other respects. Release elicited by ouabain was independent of extracellular Ca2+, was delayed for several hours by tetrodotoxin, was inhibited by reducing the concentration of extracellular Na+, and was inhibited by desipramine. These results suggest that the measured increase in transmitter release is secondary to a rise in the concentration of intracellular Na+. The data are consistent with the hypothesis that at high levels of pump inhibition, ouabain elicits nonvesicular [3H]norepinephrine release through reversal of the Na+-dependent plasma membrane carrier.
    • Grant Information:
      NS 18233 United States NS NINDS NIH HHS
    • Accession Number:
      0 (Carrier Proteins)
      37H9VM9WZL (Calcimycin)
      5ACL011P69 (Ouabain)
      71-62-5 (Veratridine)
      9NEZ333N27 (Sodium)
      EC 7.2.2.13 (Sodium-Potassium-Exchanging ATPase)
      RWP5GA015D (Potassium)
      SY7Q814VUP (Calcium)
      X4W3ENH1CV (Norepinephrine)
    • Publication Date:
      Date Created: 19850901 Date Completed: 19851017 Latest Revision: 20191210
    • Publication Date:
      20240829
    • Accession Number:
      PMC6565319
    • Accession Number:
      2993543