Neural Correlates of Inhibitory Function Following the Implicit Processing of Emotional Faces

Emotion and cognitive function interact to play a central role in determining human thought and behavior. Attention to emotion can facilitate or hinder cognitive control efforts based on the given contextual demands of the task at hand. This study used scalp electroencephalography (EEG) methods to examine the link between valence of facial stimuli and neural changes associated with emotional face processing and subsequent inhibitory response. 20 participants completed a gender discrimination stop- signal task using emotional faces. Facial valence did not differentially modulate the P200 event-related potential (ERP), indicating that happy and sad faces recruit similar neural resources in the context of implicit emotional processing. However, facial valence did significantly affect participant accuracy during response trials of gender discrimination. Trials of sad faces resulted in a higher accuracy in comparison to trials of happy faces. No significant modulation of the frontal P300 due to facial valence was observed. These results suggest that while facial valence may not modulate neural response during implicit processing of affective facial stimuli and subsequent inhibitory response, differences can be observed in behavioral response

Chronic Stress Effects on Prefrontal Cortical Structure and Function

Stressful life events have been implicated clinically in the pathogenesis of major depression, but the neural substrates that may account for this observation remain poorly understood. Attentional impairments symptomatic of depression are associated with structural and functional abnormalities in the prefrontal cortex. In three parallel rodent and human neuroimaging studies, this project assessed the effects of chronic stress on prefrontal cortical structure and function and the behavioral correlates of these changes. The first study used fMRI to elucidate the precise computational contributions of frontoparietal circuitry to attentional control in human subjects, using a task that could be adapted for rats. The results confirmed that the contributions of dorsolateral frontoparietal areas to visual attentional shifts could be dissociated from the regulatory influences of more ventrolateral areas on stimulus/response mappings, in a manner consistent with studies in animal models. They also indicated that anterior cingulate and posterior parietal cortex may act in concert to detect dissociable forms of information processing conflicts and signal to dorsolateral prefrontal cortex the need for increased attentional control. Stress-induced alterations in these regions and in the connections between them may therefore contribute to attentional impairments. The second study tested this hypothesis in rats by examining whether chronic stress effects on medial prefrontal (mPFC) and orbitofrontal (OFC) dendritic morphology underlie impairments in the behaviors that they subserve. Chronic stress induced a selective impairment in attentional control and a corresponding retraction of apical dendritic arbors in mPFC. By contrast, stress did not adversely affect reversal learning or OFC dendritic arborization. These results suggest that prefrontal dendritic remodeling may underlie the attentional deficits that are symptomatic of stress-related mental illness. The third study was designed to extend these findings to human subjects, using the techniques developed in Study 1. Accordingly, chronic stress predicted selective attentional impairments and alterations in prefrontal functional coupling that were reversible after four weeks. Together, these studies outline in broad strokes a mechanistic model by which chronic stress may predispose susceptible persons to the attentional impairments that are characteristic of major depression. Future studies will assess the roles of serotonin and neurotrophins in mediating these changes

Acetylcholine neuromodulation in normal and abnormal learning and memory: vigilance control in waking, sleep, autism, amnesia, and Alzheimer's disease

This article provides a unified mechanistic neural explanation of how learning, recognition, and cognition break down during Alzheimer's disease, medial temporal amnesia, and autism. It also clarifies whey there are often sleep disturbances during these disorders. A key mechanism is how acetylcholine modules vigilance control in cortical layer

Decoding Attentional State to Faces and Scenes Using EEG Brainwaves

Attention is the ability to facilitate processing perceptually salient information while blocking the irrelevant information to an ongoing task. For example, visual attention is a complex phenomenon of searching for a target while filtering out competing stimuli. In the present study, we developed a new Brain-Computer Interface (BCI) platform to decode brainwave patterns during sustained attention in a participant. Scalp electroencephalography (EEG) signals using a wireless headset were collected in real time during a visual attention task. In our experimental protocol, we primed participants to discriminate a sequence of composite images. Each image was a fair superimposition of a scene and a face image. The participants were asked to respond to the intended subcategory (e.g., indoor scenes) while withholding their responses for the irrelevant subcategories (e.g., outdoor scenes). We developed an individualized model using machine learning techniques to decode attentional state of the participant based on their brainwaves. Our model revealed the instantaneous attention towards face and scene categories. We conducted the experiment with six volunteer participants. The average decoding accuracy of our model was about 77%, which was comparable with a former study using functional magnetic resonance imaging (fMRI). The present work was an attempt to reveal momentary level of sustained attention using EEG signals. The platform may have potential applications in visual attention evaluation and closed-loop brainwave regulation in future