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Inhibitory and facilitatory intracortical pathways regulating motor cortical output can be studied non-invasively in humans with transcranial magnetic stimulation. These circuits include short-interval intracortical inhibition (SICI), long-interval intracortical inhibition (LICI) and intracortical facilitation (ICF). Stimulation of the motor cortex also inhibits the contralateral motor cortex (interhemispheric inhibition, IHI) at short (∼10 ms, IHI10) or long intervals (∼40 ms, IHI40). We investigated how SICI, ICF, and LICI influence IHI10 and IHI40. We hypothesize that intracortical circuits will have similar effects on IHI and cortical output neurons: SICI and LICI will decrease IHI, and ICF will increase it. Motor evoked potentials were recorded from the first dorsal interosseous muscles bilaterally in 10 healthy subjects. We compared IHI10 and IHI40 alone to IHI10 and IHI40 elicited in the presence of SICI, ICF, or LICI. Our results showed that SICI and LICI reduced IHI10, IHI40 and corticospinal output to a similar degree. ICF increased corticospinal output but had no effect on either IHI10 or IHI40. The different effects of ICF on corticospinal excitability and IHI suggest the transcallosal fibres mediating IHI and the corticospinal output system arise from different neuronal populations. SICI and LICI produce more global inhibition with similar effects on the transcallosal and descending corticospinal circuits.
Transcranial magnetic stimulation (TMS) can been used to study different inhibitory and excitatory circuits in the human motor cortex (Rothwell, 1997; Hallett, 2000; Chen, 2004). Two types of cortico-cortical inhibition are short-interval intracortical inhibition (SICI) and long-interval intracortical inhibition (LICI). SICI is elicited by a subthreshold conditioning stimulus (CS) followed by a test stimulus (TS) at interstimulus intervals (ISI) of 1–6 ms (Kujirai et al. 1993; Chen et al. 1998). LICI differs with respect to stimulus strength and ISI requiring a suprathreshold CS at an ISI of 50–200 ms (Valls-Sole et al. 1992; Wassermann et al. 1996). It is thought that SICI is mediated by GABAA receptors (Ziemann et al. 1996a; Hanajima et al. 1998) while LICI is mediated by GABAB receptors (Werhahn et al. 1999). In addition to inhibitory cortico-cortical circuits there are facilitatory pathways. One such circuit is termed intracortical facilitation (ICF) elicited by similar parameters to SICI, with a subthreshold CS, but at ISIs of 8–30 ms (Kujirai et al. 1993).
Motor cortex stimulation also inhibits the output of the contralateral motor cortex. This interhemispheric inhibition (IHI) may be responsible for suppressing activity of the contralateral hemisphere to achieve hemispheric dominance while executing motor tasks. IHI can be measured by a paired pulse paradigm, a CS delivered to the contralateral motor cortex preceding the TS by 6–50 ms (Ferbert et al. 1992; Gerloff et al. 1998; Hanajima et al. 2001; Chen et al. 2003), or by the ipsilateral silent period (iSP) (Kujirai et al. 1993; Meyer et al. 1995; Trompetto et al. 2003), which refers to interruption of ongoing voluntary electromyographic (EMG) activity following stimulation of the ipsilateral motor cortex. IHIs at ISIs of 10 ms (IHI10) and 40 ms (IHI40) are probably mediated by different mechanisms (Chen et al. 2003). The neurotransmitter systems responsible for IHI have not been established, but IHI40 may be related to LICI (Kukaswadia et al. 2005), which is probably due to GABAB mechanisms. Reductions in IHI10 have been demonstrated in several neurological and psychiatric disorders, such as schizophrenia (Daskalakis et al. 2002a), as well as in musicians who have trained from a young age (Ridding et al. 2000).
By characterizing the interactions between intracortical circuits and IHI, we can better understand the effects of abnormal intracortical circuits observed in disease states on activities of the contralateral hemisphere. Daskalakis et al. (2002b) studied how IHI interacts with intracortical circuits in the target hemisphere. It was found that IHI10 inhibits SICI and LICI reduces IHI10. Only one study examined how intracortical inhibitory circuits interact with transcallosal projections in the originating hemisphere. Trompetto et al. (2004) reported that SICI reduced the iSP area, suggesting that it suppresses the transcallosal motor output. However, the effects of SICI and ICF on IHI measured by the paired pulse method, and the effects of LICI have not been studied. We hypothesize that inhibitory and facilitatory circuits will produce widespread changes in the motor cortex, with similar effects on the corticospinal projections and the transcallosal projections.