“…On one hand, previous neuroscientific research addressing coercion has shown that anxiety and/or fear congeals cognitive resources and hampers cognitive functions, in such a way that the participants who obeyed orders did not subjectively experience their actions as voluntary ones, but rather as passive movements devoid of any sense of agency ( Caspar et al, 2016 , 2018 , 2020a , 2020b , 2021 ). At a neural level, this was observed as a reduction in the auditory N1 ERP component amplitude when the subject was under coercion, relative to the condition where he could choose freely to perform an action; thus, the brain engaging in a decrement of sensory processing in anticipation of the action outcomes, and which, again, translates into perceiving the repercussions of actions executed under coercive pressure as if they had been triggered passively ( Caspar et al, 2016 , 2021 ). On the other hand, studies exploring the neural origin of the N1 component, did so by isolating glutamatergic receptor function through micro-injections of the somatosensory barrel cortex (S1BF) in anesthetized rats with sub-convulsive concentrations of the competitive gamma-aminobutyric acid (GABA A ) receptor antagonist bicuculline methiodide (BMI) ( Krishek et al, 1996 ; Ueno et al, 1997 ; Jones and Barth, 2002 ; Johnston, 2013 ); and with the results showing that the greater the suppression of inhibition by the BMI, the broader and larger the N1 pulse width and amplitude became, respectively ( Bruyns-Haylett et al, 2017 ).…”