Voltage-dependent sodium channels in synaptoneurosomes: studies with22Na+ influx and [3H]saxitoxin and [3H]batrachotoxinin-A 20-α-benzoate binding. Effects of proparacaine isothiocyanate

Inhibition by propofol of [3H]‐batrachotoxinin‐A 20‐α‐benzoate binding to voltage‐dependent sodium channels in rat cortical synaptosomes

“…The pattern of inhibition by propofol of neurotoxin binding to Na' channels is similar to that obtained for therapeutic concentrations of local anesthetics, class I anticonvulsants, and class I antiarrhythmic drugs (Catterall, 1981;Willow & Catterall, 1982;Creveling et al, 1983;Postma & Catterall, 1984;Gusovsky et al, 1990 (Catterall, 1981). Evidence from electrophysiological studies revealed that these drugs inhibit Na+ channels in a voltage-and frequency-dependent manner by preferential interaction with the inactivated state of the channel, as described by the modulated receptor hypothesis (Catterall, 1987).…”

Irreversible inhibition of sodium current and batrachotoxin binding by a photoaffinity-derivatized local anesthetic.

“…When exposed to UV light, DNB-AB irreversibly affects both INa and [3H]-BTX binding, two assays associated with conventional LAs. Prior studies of model local anesthetics which form covalent cross-linking to the site of physiologic activity have used only inhibition at [3H]-BTX-B binding as an assay at local anesthetic activity (Gusovsky, Nishizawa, Padgett, McNeal, Rice, Kim, and Creveling, 1990;Creveling, Bell, Burke, and Chang, 1990). This ligand, DNB-AB, with a relatively high affinity and an apparently strong state-dependent selectivity for Na + channels, should prove useful in biochemical studies of the LA binding site(s).…”