Ultraviolet irradiation produces loss of saxitoxin binding to sodium channels in rat synaptosomes.
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.
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
D007473:Ion Channels; D012530:Saxitoxin; D012964:Sodium