“…Furthermore, in preliminary studies, the Ca2 -channel antagonist, nitrendipine, effectively inhibited the [3H]FNZ photoaffinity labeling of the ,uM BZ binding sites. These results indicate that the Ca2+-channel antagonist properties of the BZs are mediated by the Plasma concentrations of DZ that produce clinical effects in rats and humans range from 0.05 to 50 ,uM (26)(27)(28), and the brain levels of DZ and other BZs were shown to be 2-8 times higher than corresponding blood concentrations in the mouse, rat, and guinea pig (29,30 (31), inhibiting maximal electric-shock-induced seizures in animals (13), and preventing kindling in rats (32). At submicromolar concentrations, DZ is effective in binding to nM BZRs but has no significant clinical effects on maximal electric-shockinduced seizures, kindling, or tonic-clonic seizures in humans (13,(29)(30)(31)(32) …”