Batrachotoxin-induced depolarization and [3H]batrachotoxinin-a 20 alpha-benzoate binding in a vesicular preparation from guinea pig cerebral cortex.

摘要: The sodium channel-specific agent batrachotoxin (BTX) has been shown to induce a time- and concentration-dependent depolarization of vesicular preparation from guinea pig cerebral cortex. K0.5 for by BTX was 0.011 microM at 30 min. Membrane potential determined the equilibrium distribution [3H]triphenylmethylphosphonium ion. A series seven local anesthetics inhibit BTX-induced competitively with Ki values ranging 0.9 dibucaine 780 lidocaine ethiodide. specific binding labeled batrachotoxinin-A 20 alpha-benzoate ([3H]BTX-B) voltage-sensitive channels in preparations mouse cortex presence scorpion venom measured found yield range Kd 25 nM Bmax 0.5 1.0 pmole/mg protein; same 13 56 0.8-2.2 pmoles/mg protein. 14 [3H]BTX-B 0.6 400 benzocaine. rank order potency as antagonists follows: greater than tetracaine bupivacaine diphenhydramine piperocaine cocaine procaine quaternary anesthetic dimethyl-di(phenylcarbamoylmethyl)ammonium chloride comparable tetracaine. relative tested both paradigms were similar exception ethiodide, which 18 times more potent an inhibitor it BTX-elicited depolarization.