Mouse brain synaptosomal sodium channels: activation by aconitine, batrachotoxin, and veratridine, and inhibition by tetrodotoxin

• Published in: Comparative biochemistry and physiology. C, Comparative pharmacology and toxicology Vol. 77; no. 2; p. 267
• Main Authors: Ghiasuddin, S M, Soderlund, D M
• Format: Journal Article
• Language: English
• Published: England 1984
• Subjects: Aconitine - pharmacology; Animals; Batrachotoxins - pharmacology; Brain - metabolism; In Vitro Techniques; Ion Channels - drug effects; Kinetics; Male; Mice; Mice, Inbred ICR; Sodium - metabolism; Synaptosomes - metabolism; Tetrodotoxin - pharmacology; Veratridine - pharmacology
• ISSN: 0742-8413
• DOI: 10.1016/0742-8413(84)90011-2

Batrachotoxin, veratridine and aconitine, activators of the voltage-dependent sodium channel in excitable cell membranes, increase the rate of 22Na+ uptake by mouse brain synaptosomes. Batrachotoxin was both the most potent (K0.5, 0.49 microM) and most effective activator of specific 22Na+ uptake. Veratridine (K0.5, 34.5 microM) and aconitine (K0.5, 19.6 microM) produced maximal stimulations of 22Na+ uptake that were 73% and 46%, respectively, of that produced by batrachotoxin. Activation of 22Na+ uptake by veratridine was completely inhibited by tetrodotoxin (I50, 6 nM ), a specific blocker of nerve membrane sodium channels. These results identify appropriate conditions for measuring sodium channel-dependent 22Na+ flux in mouse brain synaptosomes. The pharmacological properties of mouse brain synaptosomal sodium channels described here are distinct from those previously described for sodium channels in rat brain synaptosomes and mouse neuroblastoma cells.