title: Ultraviolet irradiation produces loss of saxitoxin binding to sodium channels in rat synaptosomes.
abstract: Ultraviolet irradiation (UV) has been shown to cause an electrophysiologically measured inactivation of the rapid, transient sodium conductance system in nerve. Tritiated saxitoxin ([3H]STX) 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 dissociation constant of the remaining sites did not change. The receptor loss followed first-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. A22Na 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. We conclude that the UV inactivation of functional channels includes a modification of the STX binding-site structure.
mesh_terms: D000818:Animals; D001665:Binding Sites / Q000528:radiation effects; D007473:Ion Channels / Q000378:metabolism*; D007700:Kinetics; D008297:Male; D051381:Rats; D012530:Saxitoxin / Q000378:metabolism*; D012964:Sodium / Q000378:metabolism*; D013574:Synaptosomes / Q000378:metabolism / Q000528:radiation effects*; D014466:Ultraviolet Rays
chemical_list: D007473:Ion Channels; D012530:Saxitoxin; D012964:Sodium