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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)

Block of acetylcholine-activated ion channels by an uncharged local anaesthetic.

It is now thought that amine local anaesthetic compounds (procaine, lignocaine and related molecules) depress electrical activity in nerve and muscle cells by binding to sites within ion channels and blocking current flow. Such mechanisms have been proposed to account for the effects of these local anaesthetics on both the voltage-dependent sodium current and the postsynaptic actylcholine (ACh)-activated ionic current. Recently, strong evidence for block of ion channels by cationic drug molecules has been obtained by recording current from single ACh-activated channels in the presence of permanently charged quaternary derivatives of lignocaine. Most amine local anaesthetic compounds are, however, weak bases, present in both charged and uncharged forms at physiological pH, and some question remains as to whether a charged group is essential for blockade of ion channels. To resolve this question, we studied the action of the uncharged local anaesthetic benzocaine (ethyl-4-aminobenzoate) on postsynaptic ACh-activated endplate current and extrajunctional single channel current of frog muscle. We report here evidence that strongly suggests that benzocaine blocks ACh-activated ion channels.[1]


  1. Block of acetylcholine-activated ion channels by an uncharged local anaesthetic. Ogden, D.C., Siegelbaum, S.A., Colquhoun, D. Nature (1981) [Pubmed]
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