Figure 7. Connectivity model to explain SICI and SICF.
The connectivity model is derived from Fig. 4 in Amassian et al. (1987). The model is a gross simplification of nature but it is sufficient to explain all experimental data. It assumes that there exists one low-threshold inhibitory pathway, and high-threshold excitatory ‘I1- and late I-wave pathways’. CSN, corticospinal neurone; VD, voluntary drive. • denotes a GABAergic inhibitory interneurone, the ○s are excitatory interneurones. A, for SICI, a low-intensity S1 (indicated by the small filled arrow) and a high-intensity S2 (indicated by the large filled arrow) are used. S1 only activates the low-threshold inhibitory pathway. S2 given 1.5 ms after S1 only activates the I1- and late I-wave pathways, while the low-intensity pathway is refractory. The IPSP and EPSP from the inhibitory pathway and the ‘late I-wave pathway’ summate at the CSN at a delay of three I-wave intervals relative to the anodal D-wave latency. In some instances, S2 may activate the axon of the second-order interneurone, in particular if high intensity is used (indicated by the grey curved arrow). In this case, the EPSP from S2 would interact with the IPSP from the inhibitory pathway at the SCN two I-wave intervals later than the anodal D-wave latency. B, for SICF, a high-intensity S1 and a low-intensity S2 are used. S1 activates all pathways. S2 cannot activate any axon due to refractoriness. However, the initial axon segment of the second-order interneurone in the ‘late I-wave pathway’ (indicated by the small filled triangle adjacent to the cell soma) is hyperexcitable due to the EPSP from S1 and can be excited directly by S2. Therefore, the site of excitation by S2 ‘jumps up’ by one I-wave latency, and the facilitatory interaction between S1 and S2 lags the anodal D-wave latency by only two I-wave intervals. In some instances, S1 may activate in addition the axon of some second-order interneurones (indicated by the grey curved arrow). In this case, the initial axon segment of first-order interneurones is hyperexcitable due to the EPSP from S1 and can be excited by S2. The facilitatory interaction between S1 and S2 would then lag the anodal D-wave latency by only one I-wave interval.