The prostate gland contains numerous neuroendocrine cells that are believed to influence the function of the prostate gland. Our recent study demonstrated the expression of both α1- and α2-ARs, signaling the release of stored Ca2⁢ and the inhibition of N-type Ca2⁢ channels, respectively, in rat prostate neuroendocrine cells (RPNECs). In this study, the effects of NA on the resting membrane potential (RMP) of RPNECs were investigated using a whole-cell patch clamp method. Fresh RPNECs were dissociated from the ventral lobe of rat prostate and identified from its characteristic shape; round or oval shape with dark cytoplasm. Under zero-current clamp conditions with KCl pipette solution, the resting membrane potential (RMP) of RPNECs was between ⁣35 mV and ⁣85 mV. In those RPNECs with relatively hyperpolarized RMP (＜⁣60 mV), the application of noradrenaline (NA, 1μM) depolarized the membrane to around ⁣40 mV. In contrast, the RPNECs with relatively depolarized RMP (＞⁣45 mV) showed a transient hyperpolarization and subsequent fluctuation at around ⁣40 mV on application of NA. Under voltage clamp conditions (holding voltage, ⁣40 mV) with CsCl pipette solution, NA evoked a slight inward current (＜⁣20 pA). NA induced a sharp increase of cytosolic Ca2⁢ concentration ([Ca2⁢]c), measured by the fura-2 fluorescence, and the voltage clamp study showed the presence of charybdotoxin-sensitive Ca2⁢-activated K⁢ currents. In summary, adrenergic stimulation induced either depolarization or hyperpolarization of RPNECs, depending on the initial level of RMP. The inward current evoked by NA and the Ca2⁢-activated K⁢ current might partly explain the depolarization and hyperpolarization, respectively.