Using whole‐cell patch‐clamp methods, we tested whether ω‐toxins from Conus block voltage‐gated Ca2+ currents in teleost central neurons. The fractions ω‐CTx‐GVIA and ω‐CTx‐MVIIC, together with ω‐toxins from Agelenopsis, the dihydropyridine BAY‐K‐8644, and voltage steps, produced effects indicating three types of Ca2+ current in dissociated goldfish retinal ganglion cells. One was activated by depolarization of most cells beyond −65 mV, primed at −95 mV but not at −45 mV, reduced by Ni2+, and unchanged by conotoxins, agatoxins, or BAY‐K‐8644. The second type constituted more than three‐quarters of the total Ca2+ current in all cells, and at test potentials more positive than −30 mV, was reduced consistently by ω‐CTx‐GVIA, ω‐CTx‐MVIIC, and ω‐Aga‐IA, but not ω‐Aga‐IVA. The third Ca2+ current type was augmented by BAY‐K‐8644 at test potentials as negative as −45 mV, even in the presence of ω‐CTx‐GVIA. Replacement of extracellular Ca2+ by Ba2+ augmented current amplitude and slowed current decay. Conditioning depolarizations reduced Ca2+ current amplitude less than did ω‐CTx‐GVIA, and slowed current decay to imperceptible rates. These results provide the first description of conotoxin‐sensitive, voltage‐gated Ca2+ current recorded from teleost central neurons. Although most of the high‐threshold Ca2+ current in these cells is blocked by ω‐CTx‐GVIA, it is also Ni2+‐sensitive, and relatively resistant to ω‐Aga‐IIIA. The voltage sensitivities of low‐ and high‐threshold Ca2+ current may suit current recruitment in situ after light‐evoked hyperpolarizations end, and after light‐evoked depolarizations begin, respectively. © 1996 John Wiley & Sons, Inc.