The initial requirement for drug action is adequate drug delivery to the target site. This depends largely on blood flow qnd the diffusion characteristics of the drug in tissue. The drug targets collagen (a structural protein).
The pharmacological target of typical absence drugs, especially ETX, has been a matter of long-standing controversy. In line with the IT dependence of tha lamocortical slow oscillations, the mechanism of action of ETX had initially been attributed total ⅞⁸ a reduction of this current in TC neurons. Subsequent work has failed to reproduce the finding of ETX induced IT reduction by therapeutically relevant concentrations (0.25–0.75 mM). Instead, the mechanism of ETX action has been attributed to a reduction of INaP and the Ca2+-activated K+ current (IKCa). Recently, the issue was readdressed by showing that a specific IT antagonist was able to inhibit thalamic oscillations in vitro, and by showing that ETX blocks cloned IT channels expressed in HEK-293 cells
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