Linked Life Data

6256486

Source:http://linkedlifedata.com/resource/pubmed/id/6256486

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
2
pubmed:dateCreated
1981-3-24
pubmed:abstractText
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.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Aug
pubmed:issn
0022-3042
pubmed:author
pubmed:issnType
Print
pubmed:volume
35
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
430-5
pubmed:dateRevised
2003-11-14
pubmed:meshHeading
pubmed:year
1980
pubmed:articleTitle
Ultraviolet irradiation produces loss of saxitoxin binding to sodium channels in rat synaptosomes.
pubmed:publicationType
Journal Article