Abstract
Ontogenesis of the convulsant (picrotoxinin or t-butylbicyclophosphorothionate (TBPS) site(s) was defined in chicken embryonic brain with the radioligands [ 35S]TBPS and [ 3H] t-butylbicycloorthobenzoate ([ 3H]TBOB). Binding of the radioligands is detectable from day 6 of incubation. The increase in binding after day 14 of incubation is due to an increase in the number of binding sites. The pharmacological properties of the embryonic recognition site(s) do not undergo significant changes during hatching based on the affinity of embryonic and chick brain membranes for [ 3H]TBOB; the rate of association and dissociation for TBOB; non-competitive inhibition of [ 3H]TBOB binding and modulation of 1R, αS-cis-cypermethrin interaction with the recognition site(s) by GABA; and inhibition of radioligand binding by endrin, picrotoxinin and TBPS. Early development and in vitro susceptibility of the recognition site to convulsive toxicants makes the embryo a possible target for a variety of drugs and environmental toxicants acting at this site.
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