Greg Hajcak’s research while affiliated with Santa Clara University and other places

Depression is characterized by impairments of cognitive systems such as significant deficits in attention, memory, and cognitive control. The P300 (or P3) event-related potential (ERP) component has been extensively investigated over the past four decades to elucidate the underpinnings of these cognitive dysfunctions. Many studies have observed reduced P300 amplitude and prolonged P300 latency in individuals experiencing depression. The current study provides a comprehensive systematic quantitative review (i.e., meta-analysis) of the depression and P300 literature from 1981 to 2023 employing PubMed and ProQuest databases. Included articles quantitatively measured depression and P300 amplitude or latency. In total, 127 studies (total N = 12,722) comprised the current analyses (i.e., 116 examining P300 amplitude and 51 examining P300 latency), resulting in 601 effect sizes (i.e., 464 depression and P300 amplitude; 137 depression and P300 latency). Robust variance meta-regression results revealed a small significant negative effect size (r = -.15) between P300 amplitude and depression even after correcting for publication bias. There was a similar small significant positive effect size (r = .15) between P300 latency and depression. Findings from moderator analyses indicated that stimulus modality, medication use, and age impacted the P300 amplitude and depression effect size; no moderators of the P300 latency and depression relationship were observed. Regarding limitations, we did not exhaustively test all possible factors that may impact P300 and depression association. The current quantitative review confirms significant differences in P300 (both amplitude and latency) attributed to cognitive dysfunctions common in depression as well as guides future study designs and methodological approaches.

Deficits in cognitive and reward‐related functions, measured via reductions in the P300 and reward positivity (RewP) event‐related potential (ERP) components, are commonly observed in adults suffering with depression. Considering higher risk for depression emerges among females in adolescence, examination of the neurological underpinnings of depression during this critical developmental period can help further elucidate our overall understanding of the etiology of depressive disorders. Therefore, the present study sought to first examine associations between doors‐locked P300 amplitude, RewP amplitude, current depression symptoms, and age in an all‐female youth sample (sample 1: n = 296; age, 8 to 14). Next, we examined these same associations, as well as sex, in a second independent sample consisting of male and female youths (sample 2: n = 605; age, 11 to 14). Blunted doors‐locked P300 was associated with higher depressive symptoms in both samples. Moreover, the association between P300 and depression was stronger among older youths in both samples. Sex further moderated this relationship in sample 2 such that smaller P300 related to greater depression only in females. There were no consistent associations between RewP amplitude and depressive symptoms in either youth sample. These findings suggest that the doors‐locked P300 component is a reliable neural correlate of depression in youth that might specifically relate to pathways linked to increased risk for depression among adolescent females.

The late positive potential (LPP), an event‐related potential reflecting affective processing, may exhibit developmental shifts in magnitude and scalp location. In the present longitudinal study, 501 youth (47.3% female; 89.4% White; 12.0% Hispanic) completed the emotion interrupt task to elicit the LPP to neutral, positive, and negative images at approximately 9, 12, 15, and 18 years old (data collected 2010–2022). Multilevel growth models indicated an initial decrease in the occipital LPP and an increase in the parietal and central LPP during late childhood, with rates of change leveling off across adolescence. Trial condition (i.e., valence) significantly impacted trajectories only when the LPP was measured over occipital sites. Results provide novel evidence of stability and change in the LPP across development.

Preschool-onset major depressive disorder (PO-MDD) is an impairing pediatric mental health disorder that impacts children as young as three years old. There is limited work dedicated to uncovering neural measures of this early childhood disorder which could be leveraged to further understand both treatment responsiveness and future depression risk. Event-related potentials (ERPs) such as the P300 have been employed extensively in adult populations to examine depression-related deficits in cognitive and motivational systems. Few studies examine the prospective relationships between depression and P300, especially in young children. Moreover, limited research examines the relationship between P300 with psychotherapy treatment responsiveness in youths. The current study sought to examine the prospective relationships between pre-intervention P300 (i.e., choice-locked) elicited from the doors task in depressed preschool children (i.e., PO-MDD; ages 3-to-6) with reductions in depressive symptoms after completing an 18-week long dyadic psychotherapy intervention (n = 59). We also explored relations to risk for depression assessed at a follow-up visit during preadolescence (ages 8-to-12; n = 82). Those with PO-MDD exhibiting reduced choice (doors)-locked P300 demonstrated worse treatment response to psychotherapy and were more likely to meet criteria for depression during preadolescence. Moreover, the relationship between pre-intervention P300 and later preadolescence depression was significantly mediated by response to treatment. These findings suggest that deficits in brain systems linked to the choice-locked P300 component (i.e., cognitive and motivational) might be indicative of non-responsiveness to early dyadic psychotherapeutic intervention efforts for depression which impacts risk for recurrent patterns of depression in youths.

A large number of EEG studies have identified a distinct event related potential (ERP) component during error processing known as the Error-Related Negativity (ERN). In an influential study, Hajcak and Foti (2008) explored the idea that errors could trigger defensive motivational reactions and that the ERN might forecast the intensity of defensive reactions following errors. Using a flanker task, thirty-one college-aged participants responded to the direction of a central arrow with acoustic startle probes administered pseudo-randomly throughout. Hajcak and Foti’s (2008) findings indicated the ERN is indicative of individual variations in aversive reactions to errors. This has influenced understanding of the ERN being more than a simple error detection mechanism and sheds light on how people differ in their emotional responses to mistakes. As part of the #EEGManyLabs project, an international network of laboratories, we will test the replicability of the results from this influential study. The data will later be combined to compute global effect sizes of the ERN, startle potentiation, and their interaction. Collectively, these replications will help solidify the results from this highly-cited study. Given that the ERN is an integral part of a broader neural system responding to potentially threatening stimuli, this replication will provide a more solid foundation for our understanding of error processing and its relationship to defensive reactivity.

A large number of EEG studies have identified a distinct event related potential (ERP) component during error processing known as the Error-Related Negativity (ERN). In an influential study, Hajcak and Foti (2008) explored the idea that errors could trigger defensive motivational reactions and that the ERN might forecast the intensity of defensive reactions following errors. Using a flanker task, thirty-one college-aged participants responded to the direction of a central arrow with acoustic startle probes administered pseudo-randomly throughout. Hajcak and Foti’s (2008) findings indicated the ERN is indicative of individual variations in aversive reactions to errors. This has influenced understanding of the ERN being more than a simple error detection mechanism and sheds light on how people differ in their emotional responses to mistakes. As part of the #EEGManyLabs project, an international network of laboratories, we will test the replicability of the results from this influential study. The data will later be combined to compute global effect sizes of the ERN, startle potentiation, and their interaction. Collectively, these replications will help solidify the results from this highly-cited study. Given that the ERN is an integral part of a broader neural system responding to potentially threatening stimuli, this replication will provide a more solid foundation for our understanding of error processing and its relationship to defensive reactivity.

The increased risk for psychopathology associated with interpersonal violence exposure (IPV, e.g., physical abuse, sexual assault) is partially mediated by neurobiological alterations in threat-related processes. Evidence supports parsing neural circuitry related to transient and sustained threat, as they appear to be separable processes with distinct neurobiological underpinnings. Although childhood is a sensitive period for neurodevelopment, most prior work has been conducted in adult samples. Further, it is unknown how IPV exposure may impact transient-sustained threat neural interactions. The current study tested the moderating role of IPV exposure on sustained vmPFC-transient amygdala co-activation during an fMRI task during which threat and neutral cues were predictably or unpredictably presented. Analyses were conducted in a sample of 212 community-recruited youth (M/SDage = 11.77/2.44 years old; 51.9% male; 56.1% White/Caucasian). IPV-exposed youth evidenced a positive sustained vmPFC-transient amygdala co-activation, while youth with no IPV exposure did not show this association. Consistent with theoretical models, effects were specific to unpredictable, negative trials and to exposure to IPV (i.e., unrelated to non-IPV traumatic experiences). Although preliminary, these findings provide novel insight into how childhood IPV exposure may alter neural circuity involved in specific facets of threat processing.