Bifenazate is a very selective
acaricide that controls the spider mite, Tetranychus urticae.
Bifenazate is the first example of a
carbazate acaricide. Its mode of action remains unclear.
Bifenazate and its active metabolite
diazene induce
paralysis in spider mites, suggesting that they may act on the nervous system. Here we have employed a homologue (TuGABAR) of RDL (Resistance to
dieldrin), a subunit of ionotropic γ-
aminobutyric acid (
GABA) receptor, from T. urticae to investigate the action of
bifenazate and its active metabolite
diazene on this receptor function. Although neither
acaricide showed a
GABA agonist action, 30 μM of
bifenazate or
diazene significantly enhanced the
GABA-induced response of TuGABAR in a dose-dependent manner, shifting the EC(50) of
GABA from 24.8 μM to 4.83 μM and 10.8 μM, respectively. This action demonstrates a positive allosteric modulator effect of
bifenazate on T. urticae
GABA receptors. This synergistic action is likely the result of
bifenazate binding to a site distinct from that of the
GABA binding site causing a conformational change that affects the magnitude of the
GABA response. Precisely how the observed
GABA synergist action correlates with the acaricidal activity of
bifenazate, if at all, has yet to be determined.