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Accelerated Communication

Are 910 Nicotinic Acetylcholine Receptors a Pain Target for -Conotoxins?

School of Biomedical Sciences (S.T.N., D.J.A.) and the Institute for Molecular Bioscience (R.J.C., D.J.C.), the University of Queensland, Brisbane, Queensland, Australia; and Pain Management Research Institute, Kolling Institute, University of Sydney at Royal North Shore Hospital, St. Leonards, New South Wales, Australia (H.K., M.J.C.)

The synthetic -conotoxin Vc1.1 is a small disulfide bonded peptide currently in development as a treatment for neuropathic pain. Unlike Vc1.1, the native post-translationally modified peptide vc1a does not act as an analgesic in vivo in rat models of neuropathic pain. It has recently been proposed that the primary target of Vc1.1 is the 910 nicotinic acetylcholine receptor (nAChR). We show that Vc1.1 and its post-translationally modified analogs vc1a, [P6O]Vc1.1, and [E14]Vc1.1 are equally potent at inhibiting ACh-evoked currents mediated by 910 nAChRs. This suggests that 910 nAChRs are unlikely to be the molecular mechanism or therapeutic target of Vc1.1 for the treatment of neuropathic pain.

Received for publication August 3, 2007.

Accepted for publication September 5, 2007.

Address correspondence to: David J. Adams, School of Biomedical Sciences, The University of Queensland, Brisbane, QLD 4072, Australia. E-mail: dadams{at}uq.edu.au

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