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  • Title: The calcium channel antagonist, omega-conotoxin, and electric organ nerve terminals: binding and inhibition of transmitter release and calcium influx.
    Author: Ahmad SN, Miljanich GP.
    Journal: Brain Res; 1988 Jun 21; 453(1-2):247-56. PubMed ID: 3401762.
    Abstract:
    We have previously shown that the calcium channel antagonist omega-conotoxin M-VII-A blocks neurotransmitter release from isolated nerve terminals (synaptosomes) from the electric organ of the electric ray (Yeager et al., J. Neurosci., 7 (1987) 2390-2396). We now demonstrate that a related but more readily available peptide, omega-conotoxin G-VI-A (CgTx), also blocks the release of transmitter from these terminals and, in addition, inhibits depolarization-dependent uptake of Ca2+ into these terminals. The half-maximal inhibitory concentration (IC50 for block of depolarization-evoked release and for depolarization-dependent uptake of Ca2+ are approximately 3 and 2 microM, respectively. These results suggest the inhibitory effects of CgTx are due to the inhibition of Ca2+ entry into synaptosomes through voltage-sensitive calcium channels. Assays of radioiodinated CgTx binding to electric organ synaptosomal membranes and synaptosomes appear to show a single binding site with an apparent dissociation constant (Kd) of 3-5 microM and toxin receptor densities of 290 and 52 pmol/mg protein, respectively. These CgTx receptor densities are equivalent to 6% of the total synaptosomal membrane protein and 1% of the total synaptosomal protein (assuming a molecular weight of 200 kDa for the toxin receptor). If the observed CgTx receptor densities reflect the actual densities of voltage-sensitive calcium channels in electric organ synaptosomal membranes and synaptosomes, these preparations would be the richest source of these channels yet described.
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