Inhibition of K+ permeability diminishes alpha2-adrenoceptor mediated effects on norepinephrine release

I. Zimanyi, G. Folly, E. Vízi

Research output: Contribution to journalArticle

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Abstract

The effect of two different potassium channel blockers, 4-aminopyridine (4-AP) and quinine, on the alpha2-adrenoceptor mediated modulation of norepinephrine (NE) release was investigated. Pairs of mouse vasa deferentia were loaded with 3H-norepinephrine (3H-NE), superfused continuously, and stimulated electically. 4-AP (5.3 x 10-4 M), and quinine (10-5 M) enhanced the stimulation-evoked release of tritium significantly. The electrically induced release of radioactivity was reduced by alpha2-adrenoceptor agonists (1-NE and xylazine) and enhanced by the alpha2-adrenoceptor antagonist yohimbine. Both effects were affected markedly by 4-AP or quinine: the depressant action of 1-NA and xylazine was partially antagonized and the facilitatory effect of yohimbine was completely abolished during the blockade of potassium channels. It is suggested that the blockade of potassium permeability counteracts negative feedback modulation; therefore, it seems likely that the stimulation of alpha2-adrenoceptors leads to an enhanced potassium permeability and hyperpolarization of varicose axon terminals.

Original languageEnglish
Pages (from-to)102-108
Number of pages7
JournalJournal of Neuroscience Research
Volume20
Issue number1
Publication statusPublished - 1988

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4-Aminopyridine
Adrenergic Receptors
Quinine
Permeability
Norepinephrine
Xylazine
Yohimbine
Potassium
Potassium Channel Blockers
Tritium
Potassium Channels
Presynaptic Terminals
Radioactivity

ASJC Scopus subject areas

  • Neuroscience(all)

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Inhibition of K+ permeability diminishes alpha2-adrenoceptor mediated effects on norepinephrine release. / Zimanyi, I.; Folly, G.; Vízi, E.

In: Journal of Neuroscience Research, Vol. 20, No. 1, 1988, p. 102-108.

Research output: Contribution to journalArticle

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abstract = "The effect of two different potassium channel blockers, 4-aminopyridine (4-AP) and quinine, on the alpha2-adrenoceptor mediated modulation of norepinephrine (NE) release was investigated. Pairs of mouse vasa deferentia were loaded with 3H-norepinephrine (3H-NE), superfused continuously, and stimulated electically. 4-AP (5.3 x 10-4 M), and quinine (10-5 M) enhanced the stimulation-evoked release of tritium significantly. The electrically induced release of radioactivity was reduced by alpha2-adrenoceptor agonists (1-NE and xylazine) and enhanced by the alpha2-adrenoceptor antagonist yohimbine. Both effects were affected markedly by 4-AP or quinine: the depressant action of 1-NA and xylazine was partially antagonized and the facilitatory effect of yohimbine was completely abolished during the blockade of potassium channels. It is suggested that the blockade of potassium permeability counteracts negative feedback modulation; therefore, it seems likely that the stimulation of alpha2-adrenoceptors leads to an enhanced potassium permeability and hyperpolarization of varicose axon terminals.",
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N2 - The effect of two different potassium channel blockers, 4-aminopyridine (4-AP) and quinine, on the alpha2-adrenoceptor mediated modulation of norepinephrine (NE) release was investigated. Pairs of mouse vasa deferentia were loaded with 3H-norepinephrine (3H-NE), superfused continuously, and stimulated electically. 4-AP (5.3 x 10-4 M), and quinine (10-5 M) enhanced the stimulation-evoked release of tritium significantly. The electrically induced release of radioactivity was reduced by alpha2-adrenoceptor agonists (1-NE and xylazine) and enhanced by the alpha2-adrenoceptor antagonist yohimbine. Both effects were affected markedly by 4-AP or quinine: the depressant action of 1-NA and xylazine was partially antagonized and the facilitatory effect of yohimbine was completely abolished during the blockade of potassium channels. It is suggested that the blockade of potassium permeability counteracts negative feedback modulation; therefore, it seems likely that the stimulation of alpha2-adrenoceptors leads to an enhanced potassium permeability and hyperpolarization of varicose axon terminals.

AB - The effect of two different potassium channel blockers, 4-aminopyridine (4-AP) and quinine, on the alpha2-adrenoceptor mediated modulation of norepinephrine (NE) release was investigated. Pairs of mouse vasa deferentia were loaded with 3H-norepinephrine (3H-NE), superfused continuously, and stimulated electically. 4-AP (5.3 x 10-4 M), and quinine (10-5 M) enhanced the stimulation-evoked release of tritium significantly. The electrically induced release of radioactivity was reduced by alpha2-adrenoceptor agonists (1-NE and xylazine) and enhanced by the alpha2-adrenoceptor antagonist yohimbine. Both effects were affected markedly by 4-AP or quinine: the depressant action of 1-NA and xylazine was partially antagonized and the facilitatory effect of yohimbine was completely abolished during the blockade of potassium channels. It is suggested that the blockade of potassium permeability counteracts negative feedback modulation; therefore, it seems likely that the stimulation of alpha2-adrenoceptors leads to an enhanced potassium permeability and hyperpolarization of varicose axon terminals.

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