Modulation of somatosensory evoked fields from SI and SII by acute GABAA-agonism and paired-pulse stimulation

Abstract

The purpose of the present study was to shed light on the physiology underlying somatosensory evoked magnetic fields (SEFs) by means of pharmacological manipulation with the GABAA agonist lorazepam and paired-pulse stimulation. SEFs were recorded from the primary (SI) and secondary (SII) somatosensory cortices following median nerve stimulation. Responses were obtained to single stimuli every 2 s and to paired stimuli with interpulse intervals (IPIs) of 20 ms and 100 ms. Recordings were performed in 2 sessions, once after the intravenous injection of lorazepam and once after the injection of placebo. The underlying neural generators of the response components were modelled with single equivalent current dipoles (ECDs). In the single-stimulus condition, lorazepam slightly increased the ECD strength of the 1st excitatory deflection (N20m) from the contralateral SI and reduced the strengths of the following P35m, P60m and N140m deflections from the contralateral SI and the response from the ipsilateral SII. Under placebo, paired-pulse stimulation with the IPI of 20 ms diminished all SEF components compared with single-pulse stimulation. At the IPI of 100 ms, the N20m and the P60m deflections from SI had recovered to nearly baseline levels, being consistent with recovery cycles of excitatory postsynaptic potentials (EPSPs). In contrast, the P35m and N140m, as well as the SII deflections, did not recover at 100 ms. Lorazepam had no effect on the paired-pulse depression (PPD) or recovery thereof for the N20m deflection. The attenuation of the P35m deflection by lorazepam and its lack of recovery in the 100-ms paired-pulse condition are expected behaviours of inhibitory postsynaptic potentials (IPSPs) in intracellular recordings, thus lending further support to our previous suggestion that P35m largely represents IPSPs. The lack of PPD modulation of N20m by lorazepam suggests that paired-pulse depression of the first cortical excitatory response (N20m) may be caused by mechanisms other than GABAA receptor-mediated inhibition.