Figure 1.
Schematic representation of the somatosensory ascending pathway.
The tactile information was transmitted from mechanoreceptors of the facial skin to the primary somatosensory cortex (S1). The tungsten microelectrode allowed extracellular single-unit recordings in S1, while a glass electrode performed the injection of bicuculline (BIC) in the thalamic ventral posteromedial nucleus (VPM).
Figure 2.
Needle track and diffusion area.
Left, the trail of injection electrode (pink arrow, brown track). Right, the area of BIC diffusion in VPM (pink arrow, blue halo).
Figure 3.
LFP recordings in S1 and power spectral analysis.
A, representative section of propofol-induced LFP traces in S1 before and after saline injection in VPM (n=3). B, corresponding power spectral density calculated from A. C, representative section of propofol-induced LFP traces in S1 before and after BIC injection in VPM (n=8). D, corresponding power spectral density calculated from C.
Figure 4.
Basal LFP relative power in six frequency bands (total: 1–60 Hz; delta: 1–4 Hz; theta: 4–8 Hz; alpha: 8–12 Hz; beta: 12–25 Hz; gamma: 25–60 Hz).
A, saline injection in VPM did not change the values of LFP power in all bands. B, significant rise of power were found in all bands after BIC injection in VPM. Data shown as mean ± S.E.M. (n = 8). *, p < 0.05 versus control.
Figure 5.
Four response components in SEP.
A, Time course plots of SEP responses to stimulus frequencies of 2 Hz during middle propofol anaesthesia. B, Typical SEP response with four components (N1, P1, N2, P2). Dashed lines show how the amplitude of each was calculated.
Figure 6.
SEP responses before and after injection of saline/BIC in VPM.
A and D, original traces. B, time course plots of SEP responses before and after saline injection in VPM (n=3). C, amplitudes of four components of SEP calculated from B, saline injection in VPM did not change the values of all components. C, SEP responses before and after BIC injection in VPM (n=11). D, increase in all response components were observed after BIC injection in VPM. Data shown as mean ± S.E.M. (n = 11). *, p < 0.05 versus control.
Figure 7.
Results of LFP and SEP with BIC injection in S1.
A, Schematic representation of the altered injection site (in S1 area) of BIC. B, original traces of LFP and SEP traces before and after BIC (and saline) injection in S1. C, power spectral density of LFP. D, basal LFP relative power in six frequency bands. E, time course plots of SEP responses before and after BIC (and saline) injection in S1. F, amplitudes of four components of SEP calculated from E. Data shown as mean ± S.E.M. (n = 5). *, p < 0.05 versus control.
Figure 8.
Simplified diagram of the corticothalamic loop comprised of somatosensory cortex (S1), ventral posteromedial relay nucleus (VPM) and the thalamic reticular nucleus (TRN).
(+) and (-) correspond to glutamatergic (glu) excitatory and GABAergic (GABA) inhibitory projections, respectively. Propofol may increase the GABAA-receptor-mediated synaptic inhibition and thus interrupting the thalamocortical transmission.