Ultraviolet irradiation produces loss of saxitoxin binding to sodium channels in rat synaptosomes.
Publication/Presentation Date
8-1-1980
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.
Volume
35
Issue
2
First Page
430
Last Page
435
ISSN
0022-3042
Published In/Presented At
Weigele, J. B., & Barchi, R. L. (1980). Ultraviolet irradiation produces loss of saxitoxin binding to sodium channels in rat synaptosomes. Journal of neurochemistry, 35(2), 430–435. https://doi.org/10.1111/j.1471-4159.1980.tb06283.x
Disciplines
Diagnosis | Medicine and Health Sciences | Other Analytical, Diagnostic and Therapeutic Techniques and Equipment | Radiology
PubMedID
6256486
Department(s)
Department of Radiology and Diagnostic Medical Imaging
Document Type
Article