Effects of noradrenaline on the membrane potential of prostatic neuroendocrine cells of rat

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.