Growth hormone release in goldfish is partly dependent on voltage-sensitive Ca 2+ channels but somatotrope electrophysiological events affecting such channel activities have not been elucidated in this system. The electrophysiological properties of goldfish somatotropes in primary culture were studied using the whole-cell and amphotericin B-perforated patch-clamp techniques. Intracellular Ca 2+ concentration ([Ca 2+] i) of identified somatotropes was measured using Fura-2/AM dye. Goldfish somatotropes had an average resting membrane potential of −78.4 ± 4.6 mV and membrane input resistance of 6.2 ± 0.2 GΩ. Voltage steps from a holding potential of −90 mV elicited a non-inactivating outward current and transient inward currents at potentials more positive than 0 and −30 mV, respectively. Isolated current recordings indicate the presence of 4-aminopyridine- and tetraethylammonium (TEA)-sensitive K +, tetrodotoxin (TTX)-sensitive Na +, and nifedipine (L-type)- and ω-conotoxin GVIA (N-type)-sensitive Ca 2+ channels. Goldfish somatotropes rarely fire action potentials (APs) spontaneously, but single APs can be induced at the start of a depolarizing current step; this single AP was abolished by TTX and significantly reduced by nifedipine and ω-conotoxin GVIA. TEA increased AP duration and triggered repetitive AP firing resulting in an increase in [Ca 2+] i, whereas TTX, nifedipine and ω-conotoxin GVIA inhibited TEA-induced [Ca 2+] i pulses. These results indicate that in goldfish somatotropes, TEA-sensitive K + channels regulate excitability while TTX-sensitive Na + channels together with N- and L-type Ca channels mediates the depolarization phase of APs. Opening of voltage-sensitive Ca 2+ channels during AP firing leads to increases in [Ca 2+] i.