Detail of "24345-16-2"

Reference

Interactions of the neurotoxin apamin with a calcium-activated potassium channel in primary neuronal cultures

Interactions of the neurotoxin apamin with a calcium-activated potassium channel in primary neuronal cultures. Seagar, Michael J.; Granier, Claude; Couraud, Francois (Lab. Biochim., Inst. Natl. Sante Rech. Med., Marseille 13326/15, Fr.). J. Biol. Chem., 259(3), 1491-5 (English) 1984. CODEN: JBCHA3. ISSN: 0021-9258. DOCUMENT TYPE: Journal CA Section: 4 (Toxicology) 125I-labeled apamin [24345-16-2] bound to specific sites on cultured rat embryonic neurons. The dissocn. const. for the receptor-neurotoxin complex measured at equil. was 60-120 pM at pH 7.2 and 4°, with a maximal binding capacity of 3-8 fmol/mg cell protein. Apamin inhibited Ca ionophore-induced 86Rb+ release from cell cultures. The dose-effect curve for this pharmacol. test corresponded closely to the displacement of [125I]apamin by native apamin in binding expts. Formation of the [125I]apamin receptor complex requires exogenous K+. Reduced binding in the absence of K+ was due to diminished binding capacity rather than a lower affinity. The apamin receptor seems to be assocd. with a cell surface K+ site which shows 50% occupancy at 1.6 mM, and which could be involved in the regulation of channel activity. Apamin sites were present at the earliest developmental stage tested and their no. did not evolve during 8 days in culture. In the same period, however, a-scorpion toxin binding increased by a factor of 10. The ontogenesis of Ca2+-activated K+ channels does not seem to occur in parallel with that of voltage-sensitive Na+ channels.

Apamin-resistant post-stimulus hyperpolarization in the circular muscle of the guinea pig ileum

Apamin-resistant post-stimulus hyperpolarization in the circular muscle of the guinea pig ileum. Niel, Jean Pierre; Bywater, Robert A. R.; Taylor, Grahame S. (Dep. Physiol., Monash Univ., Clayton 3168, Australia). J. Auton. Nerv. Syst., 9(2-3), 565-9 (English) 1983. CODEN: JASYDS. DOCUMENT TYPE: Journal CA Section: 2 (Mammalian Hormones) The inhibitory junction potential induced in ileum strips by transmural nerve stimulation was abolished by treatment with the bee venom neurotoxin apamin [24345-16-2], and this was followed by 2 post-stimulus depolarization phases (a fast phase and a slow phase). When these studies were performed in the presence of substance P [33507-63-0], however, the fast post-stimulus depolarization was abolished to unmask a slow hyperpolarizing response which preceded the slow-phase depolarization. The slow hyperpolarizing response was slower in onset and of lesser amplitude than the inhibitory junction potential abolished by apamin, suggesting the presence of an addnl. type of hyperpolarizing response that could mediate inhibition of gastrointestinal smooth muscle.