Conotoxin-sensitive and conotoxin-resistant Ca2+ currents in fish retinal ganglion cells

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Abstract
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.