Ultraviolet Irradiation Produces Loss of Saxitoxin Binding to Sodium Channels in Rat Synaptosomes

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Abstract
UV irradiation causes an electrophysiologically measured inactivation of the rapid, transient Na conductance system in nerve. Tritiated saxitoxin ([3H]STX) [which binds at or near a region of the channel involved in ion selectivity] was used as a structural probe to assess the possibility of a corresponding perturbation in the conformation of the STX binding site. UV irradiation caused an irreversible decrease in the total number of high-affinity [3H]STX binding sites in rat synaptosomes, while the Kd of the remaining sites did not change. The receptor loss followed 1st-order kinetics, and the rate of loss was independent of temperature. The action spectrum for binding loss indicated a peak in spectral sensitivity near 280 nm. A 22Na flux assay in irradiated synaptosomes directly demonstrated that [3H]STX binding sites and veratridine-stimulated, STX-blocked 22Na efflux had similar sensitivities to UV radiation. The UV inactivation of functional channels may include a modification of the STX binding-site structure.