Overview
- Scholz, A. et al. (1998) J. Neurophysiol. 79, 1746.
Alomone Labs Lidocaine hydrochloride inhibits NaV1.2 channel currents heterologously expressed in Xenopus oocytes in an activity-dependent manner.A. Time course of current reversible inhibition by 0.5 mM Lidocaine hydrochloride (#L-145), as measured for both a non conditioned (1st) and a conditioned (2nd) stimulation. Currents were elicited by a voltage double step protocol from a holding potential of -120 mV delivered every 10 seconds (0 mV for 10 msec, -80 mV for 400 ms and again 0 mV for 100 msec). B. Example traces of the voltage protocol and current responses before and during 0.5 mM Lidocaine hydrochloride application.
Voltage-gated Na+ channels (NaV) are plasma membrane protein complexes which allow the passage of Na+ ions into cells following a change in the transmembrane voltage1,2.
NaV channels are primarily expressed in the central nervous system1,2.
Lidocaine hydrochloride is a local anesthetic of the amino amide group. Drugs of this category induce their effects by binding to the intracellular area of the Na+ channel, which blocks the channel's ability to allow Na+ to enter the nerve cell, and thus preventing the cell's depolarization3,4.
Lidocaine blocks both TTX-sensitive (NaV1.1, NaV1.2, NaV1.3, NaV1.4, NaV1.6 and NaV1.7) and TTX-resistant (NaV1.5, NaV1.8 and NaV1.9) NaV channels in DRG neurons with IC50 of 42 and 210 µM, respectively. Lidocaine is more effective in blocking the inactivated state (IC50 60 µM for TTX-resistant in the inactivated state)5.
