Absence of conditioned responding in humans: A bad measure or individual differences?

Abstract

Skin conductance response (SCR) is often used as an index of conditioned fear. SCR has been shown to be highly variable, and absence of SC reactivity is sometimes used as criteria for excluding data. It is, however, possible that low or no SC reactivity is the result of a distinct biological signature that underlies individual differences in SCR reactivity. This study examined neural correlates associated with the near absence of SCR conditionability. Archival data from 109 healthy adults aged 18–60 years were pooled. All individuals had participated in a fear conditioning protocol in a fMRI environment, during which two cues were partially reinforced (CS+) with a shock and a third cue was not (CS−). Using SCR to the conditioned stimuli and differential SCR (CS+ minus CS−), we created two groups of 30 individuals: low conditioners (defined as those showing the smallest SCR to the CS+ and smallest differential SCR) and high conditioners (defined as those showing the largest SCR to the CS+ and largest differential SCR). Our analyses showed differences in patterns of brain activations between these two groups during conditioning in the following regions: dorsal anterior cingulate cortex, amygdala, subgenual anterior cingulate cortex, and insular cortex. Our findings suggest that low or absent SCR conditionability is associated with hypoactivation of brain regions involved in fear learning and expression. This highlights the need to be cautious when excluding SCR nonconditioners and to consider the potential implications of such exclusion when interpreting the findings from studies of conditioned fear.

Altered psychophysiological correlates of risk‐taking in borderline personality disorder

“…In order to investigate whether individuals with BPD differ from HCs in their SCRs during risk‐taking, we fitted a linear mixed‐effects trial‐by‐trial model (model 1) with random intercepts for participants. We did not exclude any “non‐responders”, since a lack of SCRs to stimuli or only small variations of SCR may be the product of biological processes that underlie individual differences in SCR (Marin et al, ). We fitted the model applying restricted maximum likelihood for the estimation of variance components using the R (R Core Team, ) package lme4 (Bates, Mächler, Bolker, & Walker, ).…”

Strengthened Hippocampal Circuits Underlie Enhanced Retrieval of Extinguished Fear Memories Following Mindfulness Training

“…Although we were able to replicate previous research findings (14) by demonstrating a positive association between extinction retention and hippocampal activation at baseline with a rather small sample, we lacked statistical power to detect improvements in extinction retention following mindfulness training using skin conductance responses. Future studies may utilize other metrics and/or criteria for computing an index of extinction retention (70). Additionally, the current sample included highly stressed but healthy individuals; future studies should investigate extinction recall following mindfulness training in patient populations and using personally relevant fear-inducing cues.…”

Psychophysiological approaches to understanding the impact of trauma exposure

“…In addition, two translational studies with healthy individuals focus on elucidating mechanisms of fear acquisition and expression. These involve identifying structural brain features (gray matter volume) associated with stressful/traumatic memory formation ( Gvozdanovich, Stämpfli, Seifritz, & Rasch, 2019) and sympathetic nervous system responding during fear conditioning ( Marin et al, 2019).…”

“…Of note, machine learning analyses of the insula connectivity patterns correctly classified 80% of the sample into the nosologically defined subtypes. The crucial role of the insula and amygdala (together with the anterior cingulate cortex) is emphasized by Marin et al (2019), who document a relationship between hypoactivation in these structures and an absent skin conductance response in a classical fear‐conditioning paradigm in healthy participants. Notably, this result directs attention to biological, multimodal modulators of fear learning during or following trauma exposure.…”