Modulation of Short-Latency Afferent Inhibition Depends on Digit and Task-Relevance

Abstract

Short-latency afferent inhibition (SAI) occurs when a single transcranial magnetic stimulation (TMS) pulse delivered over the primary motor cortex is preceded by peripheral electrical nerve stimulation at a short inter-stimulus interval (∼20–28 ms). SAI has been extensively examined at rest, but few studies have examined how this circuit functions in the context of performing a motor task and if this circuit may contribute to surround inhibition. The present study investigated SAI in a muscle involved versus uninvolved in a motor task and specifically during three pre-movement phases; two movement preparation phases between a “warning” and “go” cue and one movement initiation phase between a “go” cue and EMG onset. SAI was tested in the first dorsal interosseous (FDI) and abductor digiti minimi (ADM) muscles in twelve individuals. In a second experiment, the origin of SAI modulation was investigated by measuring H-reflex amplitudes from FDI and ADM during the motor task. The data indicate that changes in SAI occurred predominantly in the movement initiation phase during which SAI modulation depended on the specific digit involved. Specifically, the greatest reduction in SAI occurred when FDI was involved in the task. In contrast, these effects were not present in ADM. Changes in SAI were primarily mediated via supraspinal mechanisms during movement preparation, while both supraspinal and spinal mechanisms contributed to SAI reduction during movement initiation.

Attention modulates specific motor cortical circuits recruited by transcranial magnetic stimulation

“…Nonetheless, the attentional dissociation observed here is consistent with a differential functional role of afferent input to the PA and AP I-wave circuits. PA SAI is reduced during finger movement with the reduction onset occurring during the preparatory phase (Asmussen et al, 2013) and involved in the surround inhibition of muscles not involved in the planned movement (Voller et al, 2006; Asmussen et al, 2014) suggesting a role in spatial and temporal priming of actions. Again, very little research has investigated the functional significance of the AP circuit however, the selective sensitivity of AP SAI to our attention manipulation is consistent with a modulatory mechanism that provides a substrate for cognitive influence upon selected actions.…”

“…Further, the positive relationship between the N20-P25 somatosensory evoked potential (SEP) and magnitude of SAI suggests that at least part of the network mediating SAI is dependent upon thalamo-cortical projections to somatosensory cortex (Bailey et al, 2016). Although there is a strong relationship between somatosensory afference and SAI, SAI is a malleable phenomenon modulated by movement timing and the relevance of a muscle to voluntary movement (Voller et al, 2006; Asmussen et al, 2013; Asmussen et al, 2014). Central cholinergic involvement, in addition to GABA A , in the generation of SAI (Ziemann et al, 2014) makes it a potential method to probe the effect of cognition on motor cortex excitability through attention-related afferent modulation.…”

Effects of lorazepam and baclofen on short‐ and long‐latency afferent inhibition

“…J Physiol 596.21 movement planning (Voller et al 2005(Voller et al , 2006Richardson et al 2008;Ni et al 2011;Asmussen et al 2013Asmussen et al , 2014Cho et al 2016). We recently reported that there is no significant relationship between afferent inhibition and tactile or motor performance (Turco et al 2018b).…”

PDGF Modulates Synaptic Excitability and Short-Latency Afferent Inhibition in Multiple Sclerosis

“…Indeed, alterations of SAI have been observed in association with cognitive deficits [46][47][48], movement preparation [49], modifications of cholinergic [48], GABAergic [50] and dopaminergic activity [51]. This may also account for the weak, although significant, correlation that we here report between SAI and PDGF-CSF.…”