The TMS-evoked potential as a measure of cortical excitation and inhibition during cognitive processes

ABSTRACT Non-invasive recordings of human brain activity – be it of BOLD or neural field potentials – all share a common, insurmountable weakness: it is impossible to identify whether amplitude changes to these signals are due to the

excitation or inhibition of their neural generators (i.e., the underlying patches of cortex). Hence, there is a critical need to develop non-invasive measures of the moment-to-moment physiological excitability of the human cortex. Such a method exists for primary motor cortex. The TMS-induced motor evoked potential (MEP) in the

electromyogram indexes the physiological excitability of cortico-motor tracts originating in primary motor cortex (M1). The MEP increases alongside motor-neuron firing during movement preparation and decreases alongside reductions in M1 firing during movement cancellation. Here, we aim to test whether a signal with similar

properties can be derived outside of M1. Specifically, we aim to test whether the TMS-evoked potential (TEP) in EEG recordings from human cortex similarly reflects changes in the cortical excitability of that underlying cortex evoked by cognitive processes. The TEP is an EEG amplitude deflection that occurs after single pulses

of TMS applied anywhere on the brain. We will use a cognitive task to differentially induce the excitation and inhibition of the same cortical region outside of M1: the frontal eye fields (FEF). The firing rate of FEF neurons is known to increase during memory- guided saccades and decrease during the anticipation of anti-saccades (while notably, non-invasive BOLD

recordings show signaling increases in both conditions). We will perform an MRI-guided, sham-controlled investigation of combined EEG and TMS to test whether the TEP – unlike fMRI or EEG – faithfully indexes these changes in task-related neuronal firing. If so, this work would provide fundamentally novel, original method to

non-invasively measure the excitability and inhibition of cortical areas outside of M1.