童年创伤与快感缺失：海马体与奖赏回路连接的研究

研究想回答的问题

快感缺失不只是“高兴不起来”。心理学通常把它分成两类：一是当下体验愉悦的能力下降，称为消费性快感缺失；二是对未来的奖励缺少期待和追求动力，称为预期性快感缺失。后者更接近动机问题，也是这项新研究关注的重点。

过去关于快感缺失的脑成像研究多集中在纹状体等奖赏区域。但动物研究提示，负责记忆与新颖性检测的海马体可能是奖赏回路的上游调节者：遇到陌生事物时，海马体通过多级神经通路影响腹侧被盖区和伏隔核，促使多巴胺释放，推动探索和目标导向行为。海马体又密集分布着与皮质醇等压力激素结合的受体，因此早期压力可能改变它的发育和功能。坦普尔大学的Kathleen J. O’Brien、俄勒冈大学的Vishnu Murty等人想检验：海马体与奖赏中枢之间的沟通是否与童年创伤共同作用，解释预期性快感缺失的个体差异。

研究怎么做

参与者来自费城一项考察年轻人精神病风险的项目，最终有92人提供可用的静息态脑扫描，80人提供可用的任务态扫描，年龄18至30岁，平均约21岁。研究者用童年创伤问卷简版测量16岁前的情绪虐待、情绪忽视和身体忽视，用时间性愉悦体验量表分别测量预期性与消费性愉悦，分数越低表示快感缺失越重。

扫描聚焦海马体前部，即与奖赏回路连接最密集的前三分之一。静息态扫描约5.8分钟，测量海马前部与伏隔核、腹侧被盖区活动的同步程度。任务态中，参与者先熟悉80张户外场景照片，再在扫描仪里观看快速闪现的图片，看到特定目标风景时按键；混入的80张全新场景用来测量海马体对新颖性的反应，研究者还用前向预测模型检验海马体对新奇图像的反应能否预测随后腹侧被盖区的活动。

主要发现与边界

对消费性快感缺失，四项脑指标都没有显著关联，也没有与创伤的交互作用。对预期性快感缺失，童年创伤与其中三项指标出现交互：在创伤水平高于样本均值一个标准差的参与者中，海马前部与伏隔核静息连接越弱、海马体对新奇场景反应越钝、海马体反应与随后腹侧被盖区活动之间的衔接越弱，预期性快感缺失越严重。创伤水平低于均值一个标准差的参与者中，这些关系不显著。用机器学习筛选变量后，组合模型解释预期性快感缺失得分约24%的变异，校正预测变量数量后约20%。

这些结果不能读成“童年创伤导致快感缺失”。研究是横断面设计，所有数据在同一时间点收集，无法确定先后顺序：也可能是原本的脑回路差异让某些人对早期压力更敏感，或长期压力逐渐改变海马通路。创伤测量依赖年轻人回忆童年，且因在线初筛和强制报告等伦理限制，问卷未包含身体与性虐待条目，结论只反映情绪虐待及情绪或身体忽视。样本还来自精神病风险研究，其中22人符合临床高风险标准，向一般年轻人群推广需谨慎；静息扫描不到6分钟，也短于近年神经影像学建议的更稳定估计所需时长。

作者如何理解

Murty对PsyPost表示，这项研究受到大量动物文献启发：参与新颖性处理的脑区对快感缺失很关键，但这一回路此前未被转化到人类研究中。他认为，普通人可以从中了解到早期生活压力可能让人更容易出现快感缺失，而调动以新颖性和探索为中心的回路或许能降低这种风险；他也提醒，中脑边缘系统并非只处理奖赏，还对动机、新颖性、信息寻求乃至好奇心敏感。

需要区分的是，这是作者对研究含义的解释，不是研究已经验证的干预效果。研究者并未测试通过新颖体验等方式调动这些回路能否真的减轻有创伤史者的快感缺失。团队下一步计划考察这些脑机制与个人回忆、日常情绪体验的关系。

A new brain imaging study published in The Journal of Neuroscience indicates that the way a memory-related brain region communicates with the brain’s reward centers is linked to motivational difficulties in young adults with a history of childhood trauma. Among individuals who experienced higher levels of early life adversity, weaker activity and connectivity in the hippocampus were associated with a reduced ability to look forward to pleasurable experiences. These findings suggest that targeting memory and novelty-processing circuits could offer a new avenue for addressing motivational symptoms in trauma-exposed populations.

Anhedonia is a psychological condition defined by a reduced ability to experience pleasure or a lack of motivation to pursue rewarding activities. It is a common symptom across several mental health conditions, including major depression and schizophrenia. Psychologists typically divide anhedonia into two categories: consummatory anhedonia, the inability to feel pleasure in the moment while engaging in an enjoyable activity, and anticipatory anhedonia, a diminished capacity to feel excited about or motivated to pursue future rewards.

To understand the biological roots of anhedonia, neuroscientists often examine the mesolimbic dopamine system, a network of brain structures that release and respond to the chemical messenger dopamine to drive reward-seeking behavior. Two central hubs in this network are the ventral tegmental area, a cluster of dopamine-producing neurons in the midbrain near the top of the brainstem, and the nucleus accumbens, a deep forebrain structure within the ventral striatum that processes reward and motivation. For instance, a longitudinal study covered by PsyPost in 2015 found that adolescents who experienced emotional neglect in childhood showed a drop in ventral striatum activity when receiving rewards over a two-year period, which predicted an increase in depressive symptoms.

While human brain imaging studies of anhedonia have largely concentrated on the striatum, animal research points to the hippocampus as an upstream regulator of this reward network. The hippocampus is a seahorse-shaped structure tucked deep within the temporal lobe on each side of the brain. Although best known for forming and retrieving memories, it also acts as a novelty detector. When an organism encounters something unfamiliar, the hippocampus sends signals through a multi-step neural circuit to the ventral tegmental area and the nucleus accumbens, triggering dopamine release that encourages exploration and goal-directed action.

Because the hippocampus contains a dense concentration of receptors that bind to stress hormones like cortisol, exposure to childhood abuse or neglect can alter how this structure develops and functions. In humans, a 2026 brain-mapping preprint from members of the same research group, which has not yet been peer reviewed, reconstructed the physical nerve tracts connecting the hippocampus, ventral tegmental area, and nucleus accumbens, providing structural evidence that these regions form an integrated loop supporting adaptive behavior. A study covered by PsyPost in 2022 found that people with moderate to severe childhood trauma reported more social anhedonia, a reduced interest in social connection, alongside differences in brain structure.

The research team behind the new study, led by first author Kathleen J. O’Brien of Temple University and senior author Vishnu “Deepu” Murty of the University of Oregon’s Adaptive Memory Lab, wanted 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.

To investigate this question, the researchers recruited participants from the Philadelphia site of a broader project examining psychosis risk in young adults, ensuring the sample included a wide range of anhedonia severity. Out of 102 individuals who completed functional magnetic resonance imaging scans, the final sample included 92 participants with usable resting-state brain scans (37 males and 55 females) and 80 participants with usable task-based scans (34 males and 46 females). The participants ranged in age from 18 to 30 years old, with an average age of about 21.

Participants completed a modified version of the Childhood Trauma Questionnaire Short-Form, a self-report survey assessing experiences of emotional abuse, emotional neglect, and physical neglect before age 16. They also filled out the Temporal Experience of Pleasure Scale, which uses separate subscales to measure anticipatory pleasure and consummatory pleasure. Lower scores on these scales indicate higher levels of anhedonia.

Inside the magnetic resonance imaging scanner, which measures brain activity by detecting changes in blood flow, the researchers focused on the anterior hippocampus, the front third of the structure that connects most densely with reward circuits. First, participants underwent a 5.8-minute resting-state scan while looking at a cross on a screen. This allowed the scientists to measure baseline functional connectivity, meaning how closely activity in the anterior hippocampus synchronized with activity in the nucleus accumbens and ventral tegmental area while at rest.

Next, participants completed a target-detection task designed to measure how the brain responds to novelty and pursues goals. An hour before entering the scanner, participants had been familiarized with 80 outdoor scene photographs, viewing each one six times. Immediately prior to scanning and again inside the scanner, participants were shown a single specific target landscape. During the brain scan, participants watched a sequence of images flash on the screen for two seconds each and had to press a button every time the target landscape appeared.

Mixed in with the 40 target trials were the 80 familiar scenes and 80 completely new outdoor scenes the participants had never seen before. Using this setup, the researchers measured how strongly the anterior hippocampus activated in response to the novel images compared to the familiar ones. They also used a forward-prediction model to test whether heightened hippocampal activity during novel scenes predicted stronger activation in the ventral tegmental area when the target image appeared shortly afterward.

In their statistical analyses, the researchers controlled for participant age, as age was correlated with baseline connectivity between the hippocampus and the ventral tegmental area, and they verified in follow-up tests that accounting for psychosis-risk status did not change the outcomes. Across all four brain measures, the authors found no statistically significant links or trauma interactions related to consummatory anhedonia. In other words, hippocampal circuit function did not explain differences in the ability to enjoy pleasurable activities in the moment.

For anticipatory anhedonia, however, interactions emerged 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. Among individuals with higher levels of childhood trauma (defined as one standard deviation above the sample average), weaker resting-state connectivity between the anterior hippocampus and the nucleus accumbens was associated with greater anticipatory anhedonia.

Similarly, in this high-trauma group, a blunted response in the anterior hippocampus when viewing novel scenes, as well as a weaker link between hippocampal responses to novel scenes and later activity in the ventral tegmental area during subsequent target detection, were both linked to worse anticipatory anhedonia. Among participants with lower levels of childhood trauma (one standard deviation below the average), these brain measures showed no statistically significant relationship with anticipatory pleasure.

To determine whether each of these neural measures contributed independently rather than reflecting the exact same underlying brain process, the scientists ran a machine-learning variable selection technique that removes redundant predictors and retains only the strongest ones. The resulting combined model accounted for 24 percent of the total variance in anticipatory anhedonia scores, or 20 percent after adjusting for the number of predictors in the model.

Even when evaluated simultaneously alongside overall trauma severity, both the interaction between trauma and resting hippocampus-accumbens connectivity and the interaction between trauma and task-based hippocampus-to-ventral-tegmental-area signaling remained independent predictors of anticipatory anhedonia. The interaction involving the hippocampus’s response to novel scenes was retained by the selection procedure but fell short of statistical significance in the final model, while higher trauma levels were themselves associated with greater anticipatory anhedonia.

The findings are in line with research covered by PsyPost in 2025, which found that chronic stress in mice weakened connections from the hippocampus to the nucleus accumbens and reduced reward-seeking, and that a single dose of ketamine restored both. That work examined stressed animals directly rather than brain scans and self-reported trauma in people. The authors suggest that when early life adversity coincides with weakened communication between the hippocampus and dopamine centers, the brain may struggle to use novel environmental cues to spark motivation and update expectations about future rewards.

“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,” Murty explained. “Sometimes there is a misinterpretation that these mesolimbic systems are just there for reward processing, but rather they are sensitive to motivation and behaviors like novelty, information seeking, and perhaps even curiosity.”

There are a few things to keep in mind when interpreting these results. Because the study is cross-sectional, meaning all data were collected at a single point in time, it cannot establish that childhood trauma or hippocampal alterations directly cause anhedonia. It is possible that preexisting differences in brain circuitry make certain individuals more sensitive to the emotional fallout of early stress, or that prolonged exposure to childhood stress gradually wears down hippocampal pathways over time. Longitudinal studies that track children and adolescents across development will be necessary to determine the exact sequence of events.

The study does have some other limitations. The researchers also did not test whether engaging these circuits, for instance through novel experiences, would actually lower anhedonia in people with a history of trauma. The trauma measure relied on young adults recalling their childhoods, and due to the online nature of the initial screening survey and ethical constraints regarding mandatory reporting without direct participant contact, the researchers excluded questions about physical and sexual abuse, meaning the findings specifically reflect emotional abuse and emotional or physical neglect.

In addition, the sample was drawn from a psychosis-risk study in which 22 participants met criteria for clinical high risk, so the results may differ in a general population of young adults, and replication in larger samples will be helpful given the modest statistical strength of the interaction findings.

The resting-state brain scans lasted just under six minutes, whereas recent neuroimaging standards suggest that longer scan times can yield more stable estimates of baseline brain connectivity. Future research could also expand beyond the hippocampus and midbrain to examine how other brain regions involved in emotion and decision-making, such as the amygdala and the prefrontal cortex, work together to influence motivation after early life stress.

Looking ahead, the research team plans to examine how these brain mechanisms connect to personal recall and everyday emotional life. “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,” Murty noted.

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.