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  • Title: [14C]guanidinium ion influx into Na+ channel preparations from mouse cerebral cortex.
    Author: Reith ME.
    Journal: Eur J Pharmacol; 1990 Jan 23; 188(1):33-41. PubMed ID: 2155120.
    Abstract:
    [14C]Guanidinium ion influx into Na+ channel preparations from mouse and rat cerebral cortex (purified synaptosomes, and synaptoneurosomes) was characterized and its properties were compared with those for 22Na+ influx. Tetrodotoxin-sensitive influx of [14C]guanidinium ion was stimulated by aconitine, veratridine, and batrachotoxin with a K0.5 of 7, 5 and 0.3 microM, respectively, the maximal influx being the same with all toxins. Scorpion venom shifted the activation curve of veratridine to the left, but did not increase the maximal influx. The potency of the local anesthetic drugs cocaine and tetracaine in inhibiting [14C]guanidinium ion influx depended upon the concentration of veratridine used to activate the Na+ channels. The mechanism of inhibition was of a competitive nature. Other local anesthetic drugs and cocaine congeners inhibited [14C]guanidinium ion influx with potencies very similar to those for inhibition of 22Na+ influx. The results show that [14C]guanidinium ion influx is a valid model for 22Na+ influx through voltage-dependent Na+ channels although there are some differences between the two influx assays. The guanidinium ion assay offers the convenience of the 14C isotope as compared with the strongly radiating 22Na+ isotope.
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