PURPOSE: The primary motor cortex is capable of rapid, reversible plastic changes and longer-term, more permanent reorganization. Ischemic nerve block (INB) is a model of deafferentation-induced short-term plasticity. We used transcranial magnetic stimulation to examine whether changes in the excitability of short- and/or long-interval intracortical inhibitory (SICI, LICI) or short-interval intracortical facilitatory (SICF) circuits underlie the corticospinal excitability increases observed during INB. METHODS: SICI and LICI recruitment curves, obtained by varying conditioning stimulus intensity, and SICF were measured at multiple inter-stimulus intervals (ISIs). RESULTS: Forearm flexor MEP amplitude increased during INB at the wrist; this was not accompanied by changes in SICI at ISIs of 1 or 2 ms, in SICF at ISIs of 1.2, 2.7, or 4.4 ms, or in LICI at an ISI of 80 ms, but was accompanied by an increase in LICI at an ISI of 150 ms. CONCLUSIONS: The results suggest that (1) the increased excitability of forearm flexors is not due to reduced SICI or LICI or increased SICF, and (2) LICI measured at ISIs of 80 and 150 ms are distinct processes. We discuss the importance of identifying distinct processes of LICI and speculate regarding other mechanisms that could potentially underlie INB-induced plasticity.
PURPOSE: The primary motor cortex is capable of rapid, reversible plastic changes and longer-term, more permanent reorganization. Ischemic nerve block (INB) is a model of deafferentation-induced short-term plasticity. We used transcranial magnetic stimulation to examine whether changes in the excitability of short- and/or long-interval intracortical inhibitory (SICI, LICI) or short-interval intracortical facilitatory (SICF) circuits underlie the corticospinal excitability increases observed during INB. METHODS: SICI and LICI recruitment curves, obtained by varying conditioning stimulus intensity, and SICF were measured at multiple inter-stimulus intervals (ISIs). RESULTS: Forearm flexor MEP amplitude increased during INB at the wrist; this was not accompanied by changes in SICI at ISIs of 1 or 2 ms, in SICF at ISIs of 1.2, 2.7, or 4.4 ms, or in LICI at an ISI of 80 ms, but was accompanied by an increase in LICI at an ISI of 150 ms. CONCLUSIONS: The results suggest that (1) the increased excitability of forearm flexors is not due to reduced SICI or LICI or increased SICF, and (2) LICI measured at ISIs of 80 and 150 ms are distinct processes. We discuss the importance of identifying distinct processes of LICI and speculate regarding other mechanisms that could potentially underlie INB-induced plasticity.