Sara Borgomaneri

Reactive inhibition is crucial for preventing inappropriate actions, and impairments in this ability are common in various disorders, with the underlying neural mechanisms poorly understood. To explore the neural dynamics of such an ability, we used a novel transcranial magnetic stimulation (TMS) protocol, cortico–cortical paired associative stimulation (ccPAS), to induce Hebbian spike‐timing‐dependent plasticity (STDP). Our goal was to investigate the functional relevance of key brain regions in the action inhibition network (AIN). Healthy participants underwent ccPAS targeting functional connectivity between AIN regions: pre/supplementary motor area (preSMA/SMA) to the left motor cortex (lM1), right inferior frontal gyrus (rIFG) to lM1, or right M1 (rM1) to lM1. Participants completed a stop signal task (SST) before and after ccPAS stimulation. Motor evoked potentials (MEP) were recorded during ccPAS to assess network plasticity, and resting motor threshold (rMT) was measured for global motor excitability. Reactive inhibition improved selectively in the preSMA/SMA‐lM1 group, with MEPs increasing after preSMA/SMA‐lM1 and rM1‐lM1 stimulation, suggesting facilitatory modulations. rMT correlated with behavioral improvement in the preSMA/SMA group. These findings demonstrate that ccPAS improved reactive inhibition, enhancing plasticity between preSMA/SMA and lM1, providing insights into the AIN's functional mechanism.

Fearful body expressions convey critical information that is rapidly and preferentially processed, facilitating swift motor reactions to potential dangers. Consistent evidence has shown that even the subliminal presentation of fear-related expressions can impact visual processing and autonomic responses, increasing sensory vigilance for monitoring potential threats. However, it remains unclear whether the presentation of non-visible emotional bodies modulates corticospinal excitability (CSE) in the observer. To investigate this, we asked 22 healthy participants to perform a sex discrimination task involving neutral target body postures, preceded by the brief subliminal presentation of fearful, happy, or neutral body postures. CSE was tested using Transcranial Magnetic Stimulation (TMS) at early time points (70, 90, and 110 ms) after target stimulus onset. Results showed a significant CSE reduction in the dominant hemisphere for subliminal fearful primes compared to happy and neutral primes. This CSE suppression was independent of the time of stimulation, participants’ subjective or objective awareness, metacognitive sensitivity, or personality traits. Our findings highlight an early automatic activation of the motor system in response to subliminal fearful stimuli, supporting the view that fearful expressions, even when not consciously perceived, activate basic survival mechanisms for monitoring and preparing fast motor responses to potential threats.

Efficient inhibitory control in the context of prepotent actions is vital. However, such action inhibition may be profoundly influenced by affective states. Interestingly, research indicates that action control can be either impaired or improved by emotional stimuli. Thus, a great deal of confusion surrounds our knowledge of the complex dynamics subtending emotions and action control. Here, we aimed to investigate whether negative stimuli, even when non-consciously presented and task-irrelevant, can affect action control relative to neutral stimuli. Additionally, we tested whether individual differences in intracortical excitability may predict action control capabilities. To address these issues, we asked participants to complete a modified version of the Stop Signal Task (SST) in which fearful or neutral stimuli were subliminally presented before the go signals as primes. Moreover, we assessed participants’ resting-state corticospinal excitability, short intracortical inhibition (SICI), and intracortical facilitation (ICF). Results demonstrated better action control capabilities when fearful stimuli were subliminally presented and interindividual SICI predicted stronger action inhibition capabilities. Taken together, these results shed new light on the intricate dynamics between action, consciousness, and motor control, suggesting that intracortical measures can be used as potential biomarkers of reduced motor inhibition in research and clinical settings.

The posterior superior temporal sulcus (pSTS) is a critical node in a network specialized for perceiving emotional facial expressions that is reciprocally connected with early visual cortices (V1/V2). Current models of perceptual decision-making increasingly assign relevance to recursive processing for visual recognition. However, it is unknown whether inducing plasticity into reentrant connections from pSTS to V1/V2 impacts emotion perception. Using a combination of electrophysiological and neurostimulation methods, we demonstrate that strengthening the connectivity from pSTS to V1/V2 selectively increases the ability to perceive facial expressions associated with emotions. This behavior is associated with increased electrophysiological activity in both these brain regions, particularly in V1/V2, and depends on specific temporal parameters of stimulation that follow Hebbian principles. Therefore, we provide evidence that pSTS-to-V1/V2 back-projections are instrumental to perception of emotion from facial stimuli and functionally malleable via manipulation of associative plasticity.

The dexterous control of our grasping actions relies on the cooperative activation of many brain areas. In the parietal lobe, 2 grasp-related areas collaborate to orchestrate an accurate grasping action: dorsolateral area AIP and dorsomedial area V6A. Single-cell recordings in monkeys and fMRI studies in humans have suggested that both these areas specify grip aperture and wrist orientation, but encode these grasping parameters differently, depending on the context. To elucidate the causal role of phAIP and hV6A, we stimulated these areas, while participants were performing grasping actions (unperturbed grasping). rTMS over phAIP impaired the wrist orientation process, whereas stimulation over hV6A impaired grip aperture encoding. In a small percentage of trials, an unexpected reprogramming of grip aperture or wrist orientation was required (perturbed grasping). In these cases, rTMS over hV6A or over phAIP impaired reprogramming of both grip aperture and wrist orientation. These results represent the first direct demonstration of a different encoding of grasping parameters by 2 grasp-related parietal areas.