Post‐traumatic stress disorder (PTSD) is a psychiatric disorder often characterized by the unwanted re‐experiencing of a traumatic event through nightmares, flashbacks, and/or intrusive memories. This paper presents a neurocomputational model using the ACT‐R cognitive architecture that simulates intrusive memory retrieval following a potentially traumatic event (PTE) and predicts hippocampal volume changes observed in PTSD. Memory intrusions were captured in the ACT‐R rational analysis framework by weighting the posterior probability of re‐encoding traumatic events into memory with an emotional intensity term I to capture the degree to which an event was perceived as dangerous or traumatic. It is hypothesized that (1) increasing the intensity I of a PTE will increase the odds of memory intrusions, and (2) increased frequency of intrusions will result in a concurrent decrease in hippocampal size. A series of simulations were run and it was found that I had a significant effect on the probability of experiencing traumatic memory intrusions following a PTE. The model also found that I was a significant predictor of hippocampal volume reduction, where the mean and range of simulated volume loss match results of existing meta‐analyses. The authors believe that this is the first model to both describe traumatic memory retrieval and provide a mechanistic account of changes in hippocampal volume, capturing one plausible link between PTSD and hippocampal volume.

Post-traumatic stress disorder (PTSD) is a psychiatric disorder often characterized by the unwanted re-experiencing of a traumatic event through nightmares, flashbacks, and/or intrusive memories. This paper presents a neurocomputational model using the ACT-R cognitive architecture that simulates intrusive memory retrieval following a potentially traumatic event (PTE) and derives predictions about an individual’s recovery trajectory, behavioral symptoms, and neurological effects. Memory intrusions were captured in the ACT-R framework by weighting the prior probability of re-encoding a memory by an emotional intensity term I, which captures the degree to which an event was perceived as dangerous or traumatic. A series of simulations were run in which a model performed memory retrievals under naturalistic conditions for up to two months after experiencing a simulated PTE. It was found that I had a significant effect on the probability of experiencing traumatic memory intrusions following a PTE, and that, under different conditions, the model experienced different probabilities of undergoing different recovery trajectories.

Background: A key challenge in developing new treatments for neuropsychiatric illness is the disconnect between preclinical models and the complexity of human social behavior. We aimed to integrate voluntary social self-administration into a preclinical rodent stress model, as a platform for the identification of basic brain and behavior mechanisms underlying stress-induced individual differences in social motivation. Here, we introduce an operant social stress (OSS) procedure with male and female mice, where lever presses are reinforced by freely moving social interaction with a familiar social partner across social stress exposure. Methods: OSS is composed of three phases: (i) social self-administration training, (ii) social stress concurrent with daily reinforced social self-administration testing, and (iii) post-stress operant social reward testing under both non-reinforced and reinforced conditions. We resolve social stress-induced changes to social motivation behaviors using hierarchical clustering and aggregated z-scores, capturing the spectrum of individual differences that we describe with a social index score. Results: OSS captures a range of stress-related dynamic social motivation behaviors inclusive of sex as a biological variable. Both male and female mice lever press for access to a social partner, independent of social partner coat color or familiarity. Social stress attenuates social self-administration in males and promotes social reward seeking behavior in females. Hierarchical clustering does not adequately describe the relative distributions of social motivation following stress, which we find is better described as a non-binary behavioral distribution that we define by introducing the social index score. This index is stable across individual mice. Conclusion: We demonstrate that OSS can be used to detect stable individual differences in stress-induced changes to social motivation in male and female mice. These differences may reflect unique neurobiological, cellular and circuit mechanisms not captured by preclinical models that omit voluntary social behaviors. The inclusion of volitional social procedures may enhance the understanding of behavioral adaptations promoting stress resiliency and their mechanisms under more naturalistic conditions.