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Modulatory actions of neurotransmitters on voltage-dependent membrane currents in bullfrog sympathetic neurones.

The concept that neurotransmitters are able to modulate voltage-dependent membrane currents during initiation of action potentials has been proposed on the basis of experimental evidences that catecholamine and acetylcholine (ACh) modify the configuration of action potentials of bullfrog sympathetic ganglion cells (Koketsu 1974a, b, 1977; Koketsu and Minota, 1975; Kuba and Koketsu, 1975, 1976; Minota and Koketsu, 1977). Indeed, both adrenaline (Koketsu and Minota, 1975; Minota and Koketsu, 1977) and ACh (Kuba and Koketsu, 1975, 1976) are able to depress the after-hyperpolarization and the maximum rate of fall of action potentials of these ganglion cells in the Ringer solution. Furthermore, these neurotransmitters or neuromodulators in sympathetic ganglia (Kuba and Koketsu, 1978) are able to depress the peak amplitude as well as the maximum rate of rise of Ca2+ spike potential produced in the isotonic Ca2+ solution (Kuba and Koketsu, 1976; Minota and Koketsu, 1977). These results suggested that both adrenaline and ACh depressed the K+ conductance (gK) and presumably also the Ca+ conductance (gCa) during an initiation of action potentials of sympathetic ganglion cells in the physiological condition.