A brain-imaging study published in The Journal of Neuroscience has linked the way memory-related regions in the brain communicate with reward centres to motivational difficulties in young adults who experienced childhood trauma. Among those reporting higher levels of early adversity, weaker activity and connectivity in the hippocampus were associated with a reduced ability to look forward to pleasurable experiences.
Anhedonia, the reduced capacity to experience pleasure or to pursue rewarding activities, can be grouped into two types: consummatory anhedonia, the inability to feel pleasure in the moment, and anticipatory anhedonia, the diminished motivation to seek future rewards.
Neuroscientists have long studied the mesolimbic dopamine system—a network that drives reward-seeking through dopamine signals. Central hubs include the ventral tegmental area and the nucleus accumbens. A 2015 PsyPost-covered longitudinal study found that adolescents who faced emotional neglect showed declining ventral striatal activity when rewards were received, predicting worsening depressive symptoms.
Beyond the striatum, the hippocampus acts as an upstream regulator of the reward network. This seahorse-shaped structure is a memory hub and a novelty detector. When confronted with something unfamiliar, the hippocampus relays signals to the ventral tegmental area and the nucleus accumbens, triggering dopamine release to encourage exploration and goal-directed action.
Because the hippocampus harbours many receptors for stress hormones, early abuse or neglect can alter its development and function. A 2026 brain-mapping preprint from the same research group reconstructed the physical nerve tracts linking the hippocampus with the ventral tegmental area and nucleus accumbens, outlining a connected loop that supports adaptive behaviour, while previous PsyPost coverage in 2022 noted associations between trauma and social anhedonia alongside brain structure differences.
The new study’s authors include first author Kathleen J. O’Brien of Temple University and senior author Vishnu “Deepu” Murty of the University of Oregon’s Adaptive Memory Lab, who sought to test whether disruptions in hippocampal–reward communication interact with childhood trauma to explain why some people struggle with anhedonia.
“This study was motivated by a large animal literature that suggests that regions implicated in novelty processing, like the hippocampus, are critical for anhedonia, but characterization of this circuit had not been translated into the human literature,” Murty told PsyPost.
Participants were drawn from the Philadelphia site of a broader project on psychosis risk in young adults, ensuring a wide spectrum of anhedonia severity. Of 102 individuals who completed functional magnetic resonance imaging, the final sample included 92 with usable resting-state scans and 80 with usable task-based scans. The group ranged from 18 to 30 years old, with an average age of about 21.
Participants completed the Childhood Trauma Questionnaire Short-Form to assess emotional abuse and neglect and physical neglect before age 16, and the Temporal Experience of Pleasure Scale to measure anticipatory and consummatory pleasure. Higher levels of anhedonia corresponded to lower scores on these scales.
Inside the MRI, the team focused on the anterior hippocampus, the portion most densely connected with reward circuits. A 5.8-minute resting-state scan established baseline connectivity between the anterior hippocampus and the nucleus accumbens and ventral tegmental area, while participants also completed a task designed to probe novelty processing and goal-directed action.
Before scanning, participants were familiarised with 80 outdoor scene photographs by viewing each six times. Inside the scanner, they saw a mix of 40 target landscapes, 80 familiar scenes and 80 novel scenes, and pressed a button whenever the target landscape appeared. This design allowed the researchers to gauge hippocampal responses to novel images and how these responses predicted subsequent activity in reward-related regions.
Statistical analyses controlled for age, as age correlated with baseline hippocampus–VTA connectivity, and follow-up checks showed that psychosis-risk status did not alter the results. Across all four brain measures, the study found no statistically significant links or trauma interactions with consummatory anhedonia.
By contrast, anticipatory anhedonia revealed notable interactions between childhood trauma and three of the four hippocampal circuit measures. Resting connectivity between the anterior hippocampus and the ventral tegmental area showed no such interaction, but weaker hippocampus–nucleus accumbens connectivity in the high-trauma group correlated with greater anticipatory anhedonia.
Similarly, a blunted anterior hippocampal response to novel scenes, and a weaker link between hippocampal novelty responses and later ventral tegmental area activity during the target-detection phase, were associated with poorer anticipatory pleasure in those with higher trauma exposure. In participants with lower trauma, these brain measures showed no significant association with anticipatory pleasure.
To assess whether these neural measures captured independent effects, the researchers employed a machine-learning variable-selection approach. The resulting model accounted for 24 percent of the total variance in anticipatory anhedonia scores (20 percent after adjustment for predictor count), with trauma–resting hippocampus–nucleus accumbens connectivity and trauma–task-based hippocampus–VTA signaling remaining as independent predictors. The hippocampus response to novelty was retained by the selection process but did not reach significance in the final model, while trauma itself remained linked to greater anticipatory anhedonia.
The findings echo earlier work discussed by PsyPost in 2025, which showed chronic stress in mice weakened hippocampal connections to the nucleus accumbens and dampened reward-seeking, with ketamine capable of restoring both. The researchers suggest that when early adversity coincides with weakened communication between the hippocampus and dopamine centres, the brain’s ability to use novel cues to spark motivation and update expectations about future rewards may be impaired.
Murty noted that the practical takeaway is that early life stress can heighten vulnerability to anhedonia, but engagement of circuits involved in novelty and exploration can mitigate that risk: “The average person should take away that early life stress may make you vulnerable to anhedonia, a lack of pleasure, but that engagement of circuits centered on novelty and exploration can minimize that risk.”
Several caveats should temper interpretation. The study is cross-sectional, so it cannot prove causation between childhood trauma or hippocampal changes and anhedonia. It remains possible that preexisting brain differences increase sensitivity to early stress or that prolonged adversity gradually alters hippocampal pathways. Longitudinal work tracking individuals over development will be needed to establish sequence of events.
Other limitations include the trauma measure relying on retrospective reporting and the omission of questions about physical and sexual abuse, meaning the findings specifically reflect emotional abuse and neglect. The sample came from a psychosis-risk cohort, so results may differ in the general population, and replication in larger samples would be helpful given the modest statistical strength of some interactions.
The resting-state scans lasted under six minutes, a duration that newer neuroimaging standards suggest may yield more stable connectivity estimates with longer durations. Future research could extend beyond the hippocampus and midbrain to explore how other regions involved in emotion and decision-making, such as the amygdala and prefrontal cortex, cooperate to influence motivation after early life stress.
Looking ahead, the researchers plan to investigate how these brain mechanisms relate to personal recall and daily emotional life. Murty said: “Our long-term goal is to try to understand how these findings relate to subjective experience of anhedonia, and how those might relate to memories of the past.”
The study, “Functional Integrity of Mesolimbic-Hippocampal Circuits Is Associated with Anhedonia in Individuals with Early Life Stress,” was authored by Kathleen J. O’Brien, Blake L. Elliott, Ian O’Shea, Jason Schiffman, Vijay A. Mittal, Lauren M. Ellman, and Vishnu P. Murty.
