The membrane conductance and reversal potential were determined for neurones in toad dorsal root ganglion (DRG) with intracellular recording technique during depolarization or hyperpolarization induced by noradrenaline (NA). The effects of blocking agents for potassium or calcium channels on NA-induced membrane potential responses were examined. In 15 neurones, the NA-induced depolarization was accompanied by a 32.6% decrease of membrane conductance; in other 4 neurones, the depolarization was accompanied by an initial increase and subsequent decrease in membrane conductance. The NA hyperpolarization was associated with an increase of membrane conductance by 16.2% (n = 8). The mean reversal potential of NA-induced depolarization was -88.5 +/- 0.9 mV (means +/- SE, n = 4). The NA-induced hyperpolarization was nullified at -89 to -92 mV of membrane potentials (n = 3). Tetraethylammonium superfusion enhanced NA depolarization amplitude by 73.7 +/- 11.9% (means +/- SE, n = 7) and depressed NA hyperpolarization amplitude by 40.5% (n = 4). Intracellular injection of CsCl increased phenylephrine-induced depolarization by 34.5% (n = 4). MnCl2 superfusion decreased the amplitudes of NA-induced depolarization by 50.5 +/- 9.9% (means +/- SE, n = 10), and of NA-induced hyperpolarization by 89.5 +/- 4.9% (means +/- SE, n = 7) respectively. The results suggest that the depolarization or hyperpolarization induced by NA might be mediated by the alteration in activation of K+ or Ca2+ channels.