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Inhibition of K + permeability diminishes alpha 2 ‐adrenoceptor mediated effects on norepinephrine release
Author(s) -
Zimanyi I.,
Folly G.,
Vizi E. S.
Publication year - 1988
Publication title -
journal of neuroscience research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.72
H-Index - 160
eISSN - 1097-4547
pISSN - 0360-4012
DOI - 10.1002/jnr.490200114
Subject(s) - yohimbine , chemistry , stimulation , hyperpolarization (physics) , prazosin , endocrinology , 4 aminopyridine , medicine , antagonist , norepinephrine , potassium , alpha 2 adrenergic receptor , idazoxan , xylazine , catecholamine , pharmacology , potassium channel , receptor , anesthesia , stereochemistry , dopamine , biochemistry , organic chemistry , nuclear magnetic resonance spectroscopy , ketamine
Abstract The effect of two different potassium channel blockers, 4‐aminopyridine (4‐AP) and quinine, on the alpha 2 ‐adrenoceptor mediated modulation of norepinephrine (NE) release was investigated. Pairs of mouse vasa deferentia were loaded with 3 H‐norepinephrine ( 3 H‐NE), superfused continuously, and stimulated electrically. 4‐AP (5.3 × 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 alpha 2 ‐adrenoceptor agonists (1‐NE and xylazine) and enhanced by the alpha 2 ‐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 the potassium channels. It is suggested that the blockade of potassium permeability counteracts negative feedback modulation; therefore, it seems likely that the stimulation of alpha 2 ‐adrenoceptors leads to an enhanced potassium permeability and hyperpolarization of varicose axon terminals.