Lidocaine produces a shunt in rat [correction of rats] thalamocortical neurons, unaffected by GABA(A) receptor blockade.

Low concentrations of lidocaine reversibly decrease input resistance and shunt action potentials in neurons of the ventral posterolateral thalamic nucleus (VPL) in vitro. Using differential interference contrast infrared videomicroscopy and whole-cell patch-clamp techniques in rat brain slices, we studied the effects of bicuculline methobromide to test whether the lidocaine-induced shunt in VPL neurons is mediated by GABA(A) receptors. Bicuculline (50 microM) restored tonic firing rates to control values following reduction by lidocaine (10 microM). However, bicuculline did not influence lidocaine's actions to decrease slope resistance over the voltage range from approximately -90 mV to spike threshold. Likewise, bicuculline did not affect the shunt-induced reductions of spike-afterhyperpolarizations produced by lidocaine. The results of this study imply that the effects of low lidocaine concentrations in thalamocortical neurons are not mediated by GABA(A) receptors.