Excitatory and inhibitory effects of epinephrine on neonatal rat sympathetic preganglionic neurons in vitro

Current and voltage recordings were made from antidromically identified sympathetic preganglionic neurons (SPNs) in transverse thoracolumbar spinal cord slices removed from neonatal rats. When applied by either pressure ejection or superfusion, epinephrine (Epi) caused a slow depolarization or an inward current in 62 SPNs (42%) and a slow hyperpolarization or an outward current in 21 SPNs (14%). The responses persisted in low calcium- or tetrodotoxin-containing media. The Epi-induced depolarization or inward current was associated with increased membrane resistance; it was reduced by membrane hyperpolarization and nullified at a membrane potential of about -100 mV; a clear reversal however was not observed at more negative potential levels. In a number of SPNs the Epi-induced depolarization was accompanied by small inhibitory postsynaptic potentials. The latter were eliminated by a low calcium solution and by the glycine antagonist strychnine, suggesting that they were caused by glycine or a glycine-like substance released from interneurons subsequent to activation by Epi. The Epi-induced hyperpolarization or outward current was associated with decreased membrane resistance, and nullified around -100 mV. The alpha-adrenergic antagonist, dihydroergotamine, and alpha 1-antagonist, prazosin, reversibly blocked the excitatory, whereas the alpha 2-antagonist, yohimbine, abolished the inhibitory response, respectively. It is concluded that Epi acting on alpha 1- and alpha 2-adrenergic receptors depolarizes and hyperpolarizes the rat SPNs by decreasing or increasing membrane conductances to potassium ions.