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Vol. 59, Issue 6, 1457-1463, June 2001

Novel Wasp Toxin Discriminates between Neuronal and Cardiac Sodium Channels

Eiji Kinoshita, Hiroshi Maejima, Kaoru Yamaoka, Katsuhiro Konno, Nobufumi Kawai, Eisuke Shimizu, Sawana Yokote, Hitoshi Nakayama, and Issei Seyama

Department of Physiology (E.K., K.Y., I.S.) and Institute of Health Sciences (H.M.), School of Medicine, Hiroshima University, Hiroshima, Japan; Institute of Biosciences at Rio Claro, Sao Paulo State University, Sao Paulo, Brazil (K.K.); Department of Physiology, Jichi Medical School, Tochigi, Japan (N.K.); and Department of Biofunctional Chemistry, Faculty of Pharmaceutical Sciences, Kumamoto University, Kumamoto, Japan (E.S., S.Y., H.N.)

Pompilidotoxins (PMTXs), derived from the venom of solitary wasp has been known to facilitate synaptic transmission in the lobster neuromuscular junction, and a recent further study from rat trigeminal neurons revealed that the toxin slows Na+ channel inactivation without modifying activation process. Here we report that beta -PMTX modifies rat brain type II Na+ channel alpha -subunit (rBII) expressed in human embryonic kidney cells but fails to act on the rat heart alpha -subunit (rH1) at similar concentrations. We constructed a series of chimeric mutants of rBII and rH1 Na+ channels and compared modification of the steady-state Na+ currents by beta -PMTX. We found that a difference in a single amino acid between Glu-1616 in rBII and Gln-1615 in rH1 at the extracellular loop of D4S3-S4 is crucial for the action of beta -PMTX. PMTXs, which are small peptides with 13 amino acids, would be a potential tool for exploring a new functional moiety of Na+ channels.

Copyright © 2001 by The American Society for Pharmacology and Experimental Therapeutics


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Copyright © 2001 by the American Society for Pharmacology and Experimental Therapeutics