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 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 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 the 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.
- noradrenaline release
- potassium permeability
- presynaptic modulation
ASJC Scopus subject areas
- Cellular and Molecular Neuroscience