[ 3 H]AVM B1a preferentially binds to synaptic membranes from several regions of rat brain. [ 3 H]AVM B1a specific binding to intact monolayers of granule cells increases rapidly with time of incubation and reaches equilibrium after approximately 20 min at 24°C. Higher concentrations of [ 3 H]AVM B1a leads to markedly greater nonspecific binding, 60% at 25 nM. Various AVM analogs also produce concentration-dependent inhibition of [ 3 H]AVM B1a binding in intact cerebellar neurons. AVM B1a and moxidectin are similar in potency (IC 50 values, 120 and 126 nM, respectively). AVMB1a-stimulated chloride efflux from mouse brain synaptic vesicles results from the activation of GABA-insensitive chloride channels and that this action is distinct from their previously documented effects on GABA-gated chloride channels in mouse brain preparations.
Bacteria are significantly inhibited when the AVM B1a concentration is higher than 83.3 mg/kg, while fungi are less impaired in soil. Soil respiration is also inhibited by high concentration AVM B1a, which differs with soil types. The half lethal dosage (LD 50 ) of AVM B1a to soil earthworm is estimated as 4.63 mg × cm 2 in filter paper contact test, and as 24.13 and 17.06 mg/kg, respectively after treated 7 and 14 days in artificial soil. Iin artificial soil, the LC50 of AVM B1a on earthworms are 24.1 mg/kg and 17.1 mg/kg, respectively, for 7 and 14 days. About 80.0% and 94.8% of the accumulated AVM B1a are eliminated respectively in two groups within 1 day after they are exposed to AVM B1a-free soil, but a trace amount of AVM B1a is found for a relative long time in earthworms.