Examination of the role of calcium in the adrenaline-induced hyperpolarization of bullfrog sympathetic neurons

Abstract

The adrenaline-induced hyperpolarization, which was recorded in neurons of bullfrog paravertebral sympathetic ganglia by means of the sucrose gap technique, was antagonized by 1 mM 4-aminopyridine. The response was unaffected by drugs which influence intracellular Ca 2+ movements or Ca 2+-sensitive K + conductances, i.e. 100 or 200μM Cd 2+, 60μM dantrolene Na +. 10mM tetraethylammonium bromide, 0.5–2.0μM apamin or 70μM (+)-tubocurarine chloride. The spontaneous, rhythmic hyperpolarizations which occur in ganglionic neurons in the presence of 5 m M caffeine and reflect activation of Ca 2+-sensitive K + conductances following mobilization of intracellular Ca 2+, were examined by means of intracellular recording. These responses were often biphasic, comprising a transient rapid early phase and a slow late phase. Tetraethylammonium (10 mM) and 0.5–2.μM apamin antagonized the rapid early phase and 70 μM (+)-tubocurarine chloride antagonized both phases of the response. Neither phase of these spontaneous, rhythmic, caffeine-induced hyperpolarizations were affected by 1 mM 4-aminopyridine. Although the adrenaline-induced hyperpolarization was antagonized by 50 μM 8-(diethylamino)octyl-3,4,5-trimethoxybenzoate and by 50 μM quinidine, the majority of the results argue against the hypothesis that mobilization of intracellular Ca 2+ is required for activation of the K + conductance thought to underlie the adrenaline-induced hyperpolarization.