coupling of agonist binding to gating of the ion channel, indicating that agonist binding and subsequent ion channel opening are separate, but related processes. Phy differentially displaces [125 I]a-BGT from the chimeric nAChR, suggesting that the b subunit is not involved in Phy binding, and that Phy targets the insect agonist binding loop C.
ACKNOWLEDGEMENTSWe would like to thank Dr B Schmitt (Max-PlanckInstitut fu È r Hirnforschung, Frankfurt, Germany) and Dr M Ballivet (University of Geneva, Switzerland) for kindly providing us with cDNA encoding the SAD and the chick b2 subunit, respectively.