Local anesthetics, or LAs, induce temporary loss of sensation by blocking nerve conduction in a limited region. Nerves conduct electrical signals through axons. When an axon is excited, the sodium ion channels in its membrane open. The sodium ion influx depolarizes the membrane, triggering a conformational change that inactivates the channel. This blocks the further influx of sodium ions into the cell. LAs target these sodium ion channels to prevent signal transmission. Because LAs remain uncharged and lipophilic at a physiological pH, they can cross the lipid bilayer to move into an axon. Once inside, the LA becomes protonated at the acidic pH of the axon cytoplasm. The cationic LA binds strongly to its receptor site within the sodium channel, locks the channel in its inactive conformation, and prolongs the blocking of sodium ion influx. At high concentrations, LAs bind and block more sodium channels. This prevents the neurons from transmitting an electrical signal down the axon, completely blocking nerve impulse conduction.