Archives of Toxicology

, Volume 62, Issue 4, pp 311–315

Vertebrate cyclodiene insecticide resistance: Role of γ-aminobutyric acid and diazepam binding sites

Authors

  • James C. Bonner
    • Department of Biological SciencesMississippi State University
  • James D. Yarbrough
    • Department of Biological SciencesMississippi State University
Original Investigations

DOI: 10.1007/BF00332493

Cite this article as:
Bonner, J.C. & Yarbrough, J.D. Arch Toxicol (1988) 62: 311. doi:10.1007/BF00332493

Abstract

Certain populations of the mosquitofish (Gambusia affinis) are highly resistant to cyclodiene and cyclodiene-type insecticides that competitively interact with the picrotoxinin binding site of the γ-aminobutyric acid (GABA) receptor-ionophore complex in the central nervous system. Resistance involves a reduction in affinity of the picrotoxinin binding site. The present study reports that GABA receptor binding is increased in resistant brain membranes compared to membranes from susceptible fish at concentrations of free radioligand above 0.2 μM. The increase appears to be due to a greater number of binding sites (Bmax) in the resistant population. Diazepam binding affinity (Kd) and Bmax were not different in membranes from resistant fish compared to those from susceptible fish. Up-regulation of GABA binding sites in the resistant fish population may compensate for a possible reduction of GABAergic transmission caused by chronic environmental exposure to cyclodiene insecticides. However, a lack of cross-resistance to bicuculline (a competitive GABA antagonist) indicates that an increase in GABA sites is not a mechanism of cyclodiene resistance.

Key words

Cyclodiene resistanceMosquitofishGABA receptorsDiazepam receptorsPicrotoxininEndrinBicuculline

Copyright information

© Springer-Verlag 1988