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A Novel α-Conotoxin Identified by Gene Sequencing Is Active in Suppressing the Vascular Response to Selective Stimulation of Sensory Nerves in Vivo

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Department of Biochemistry and Molecular Biology and National Ageing Research Institute, The University of Melbourne, Victoria 3010, Australia
Cite this: Biochemistry 2003, 42, 22, 6904–6911
Publication Date (Web):May 16, 2003
https://doi.org/10.1021/bi034043e
Copyright © 2003 American Chemical Society

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    Abstract

    We describe the identification of a conopeptide sequence in venom duct mRNA from Conus victoriae that suppresses a vascular response to pain in the rat. PCR-RACE was used to screen venom duct cDNAs for those transcripts that encode specific antagonists of vertebrate neuronal nicotinic acetylcholine receptors (nAChRs). One of these peptides, Vc1.1, was active as an antagonist of neuronal nAChRs in receptor binding and functional studies in bovine chromaffin cells. It also suppressed the vascular responses to unmyelinated sensory nerve C-fiber activation in rats. Such vascular responses are involved in pain transmission. Furthermore, its ability to suppress C-fiber function was greater than that of MVIIA, an ω-conotoxin with known analgesic activity in rats and humans. Vc1.1 has a high degree of sequence similarity to the α-conotoxin family of peptides and has the 4,7 loop structure characteristic of the subfamily of peptides that act on neuronal-type nAChRs. The results suggest that neuronal α-conotoxins should be further investigated with respect to their potential to suppress pain.

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     This work was supported by grants from the Melbourne Research and Development Scheme to K.R.G. and B.G.L. and from the Ageing Well Foundation, National Ageing Research Institute, to Z.K.

     Department of Biochemistry and Molecular Biology, The University of Melbourne.

    §

     National Ageing Research Institute, The University of Melbourne.

    *

     Address correspondence and reprint requests to this author. E-mail:  [email protected]. Phone:  +61-3-8344 5911. Fax:  +61-3-9347 7730.

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