title: Conotoxin-sensitive and conotoxin-resistant Ca2+ currents in fish retinal ganglion cells.
abstract: Using whole-cell patch-clamp methods, we tested whether omega-toxins from Conus block voltage-gated Ca2+ currents in teleost central neurons. The fractions omega-CTx-GVIA and omega-CTx-MVIIC, together with omega-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 omega-CTx-GVIA, omega-CTx-MVIIC, and omega-Aga-IA, but not omega-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 omega-CTx-GVIA. Replacement of extracellular Ca2+ by Ba2+ augmented current amplitude and slowed current decay. Conditioning depolarizations reduced Ca2+ current amplitude less than did omega-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 omega-CTx-GVIA, it is also Ni(2+)-sensitive, and relatively resistant to omega-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.
authors.affiliation: Section of Neurobiology, University of California, Davis 95616-8519, USA.
authors.forename: V P
authors.initials: VP
authors.lastname: Bindokas
authors.forename: A T
authors.initials: AT
authors.lastname: Ishida
mesh_terms: D001498:3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethyl-5-nitro-4-(2-(trifluoromethyl)phenyl)-, Methyl ester / Q000494:pharmacology; D060848:Agatoxins; D000818:Animals; D001464:Barium / Q000378:metabolism; D002118:Calcium / Q000378:metabolism; D002120:Calcium Channel Agonists / Q000494:pharmacology; D002121:Calcium Channel Blockers / Q000494:pharmacology*; D004095:Dihydropyridines / Q000494:pharmacology; D006054:Goldfish / Q000033:anatomy & histology*; D008564:Membrane Potentials / Q000187:drug effects; D018408:Patch-Clamp Techniques; D010455:Peptides / Q000494:pharmacology*; D012165:Retinal Ganglion Cells / Q000737:chemistry / Q000187:drug effects* / Q000502:physiology; D013111:Spider Venoms / Q000494:pharmacology; D020866:omega-Conotoxin GVIA
chemical_list: D060848:Agatoxins; D002120:Calcium Channel Agonists; D002121:Calcium Channel Blockers; D004095:Dihydropyridines; D010455:Peptides; D013111:Spider Venoms; C083855:omega-agatoxin-Aa4b; D001464:Barium; D001498:3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethyl-5-nitro-4-(2-(trifluoromethyl)phenyl)-, Methyl ester; C038806:1,4-dihydropyridine; D020866:omega-Conotoxin GVIA; D002118:Calcium