Modulatory effects of movement sequence preparation and covert spatial attention on early somatosensory input to non-primary motor areas
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Early frontal somatosensory evoked potentials (SEPs) (i.e., N30) are known to be modulated by movement. Furthermore, individuals with prefrontal lesions have enhanced early frontal SEPs. However, it is currently unclear through what mechanism the prefrontal cortex may modulate early frontal SEPs. The current study investigated whether prefrontal modulatory effects on frontal SEPs may depend on the relevancy of somatosensory input for movement (i.e., interaction with motor areas). Two experiments were conducted to determine whether selective spatial attention alone (Experiment 1-Attend and Mentally Count) or when using attended somatosensory input in the preparation of finger sequences with the limb contralateral to somatosensory stimulation (Experiment 2-Attend for Movement Preparation) could modulate SEPs. In Experiment 1, SEPs elicited by median nerve (MN) stimulation at both wrists were measured in trials when individuals attended and mentally counted vibrotactile (VibT) input at either index finger. In Experiment 2, SEPs elicited by MN stimulation at the left wrist were measured in trials when individuals used attended VibT input at the left index finger to prepare finger sequences that were contralateral to MN stimulation. In both experiments, control conditions were performed where participants received passive VibT and MN stimulation. Results from Experiment 1 confirmed that selective spatial attention alone does not modulate frontal N30 peak amplitudes. However, Experiment 2 revealed that frontal N30 peak amplitudes were decreased (i.e., gated) when individuals used attended VibT input at the left index finger to prepare contralateral finger sequences. These results support a role of sensory gating of early frontal SEPs during finger sequence preparation of the limb contralateral to MN stimulation that may result from increased activity in prefrontal, motor preparatory areas, and basal ganglia.
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