These tools will no longer be maintained as of December 31, 2024. Archived website can be found here. PubMed4Hh GitHub repository can be found here. Contact NLM Customer Service if you have questions.


Pubmed for Handhelds

PUBMED FOR HANDHELDS

Search MEDLINE/PubMed

  • Title: High-affinity and selectivity of neosurugatoxin for the inhibition of 22Na influx via nicotinic receptor-ion channel in cultured bovine adrenal medullary cells: comparative study with histrionicotoxin.
    Author: Wada A, Uezono Y, Arita M, Tsuji K, Yanagihara N, Kobayashi H, Izumi F.
    Journal: Neuroscience; 1989; 33(2):333-9. PubMed ID: 2622530.
    Abstract:
    In cultured bovine adrenal medullary cells, neosurugatoxin and histrionicotoxin inhibited carbachol-induced influx of 22Na, 45Ca and secretion of catecholamines with IC50 of 27 nM and 3 microM, respectively. The inhibitory effects of neosurugatoxin were reversed by the increased concentrations of carbachol, whereas those of histrionicotoxin were not. Histrionicotoxin at concentrations higher than 10 microM also reduced veratridine-induced influx of 22Na, 45Ca and secretion of catecholamines, while neosurugatoxin had no effects. High K-induced 45Ca influx and catecholamine secretion were not altered by either neosurugatoxin or histrionicotoxin. The present findings suggest (1) neosurugatoxin competitively inhibits nicotinic receptor-ion channel complex at nanomolar concentrations, but has no effects on voltage-dependent Na channel and voltage-dependent Ca channel; (2) histrionicotoxin at micromolar concentrations non-competitively suppresses nicotinic receptor-ion channel complex. Higher concentrations of histrionicotoxin also interferes with voltage-dependent Na channel, but has no effect on voltage-dependent Ca channel; (3) neosurugatoxin, due to its high-affinity and selectivity, may be a useful probe for studying nicotinic receptors in nervous tissues.
    [Abstract] [Full Text] [Related] [New Search]