A recent study conducted at Ohio State University has revealed that early-life stress has a greater impact on gene expression in the brain compared to childhood head injuries. The research, which utilized a rat model to mimic human early-life stress and head injury, focused on the hippocampal region and highlighted the long-term consequences of early-life stress.

The findings of this study underscore the importance of recognizing the lasting effects of early-life stress, which can contribute to risk-taking behavior and social disorders in adulthood. This emphasizes the need for effective interventions to mitigate these negative outcomes.

Interestingly, the research demonstrated that early-life stress in rats resulted in more significant changes in brain gene expression than head injuries alone. Additionally, both stress and combined stress-head injury conditions activated pathways related to brain plasticity and oxytocin signaling, indicating a period of vulnerability.

Of particular significance, only the rats subjected to early-life stress displayed increased risk-taking behavior in adulthood. This aligns with similar trends observed in human data, further highlighting the potential negative effects of early-life stress on behavior.

Lead researcher Michaela Breach, a graduate student in the lab of senior author Lenz, explained that the study provided insights into the mechanisms through which traumatic brain injury and early-life stress can impact brain development. The results suggested that the impact of stress should not be underestimated when considering the developing brain.

The study utilized a rat model where newborn rats were temporarily separated from their mothers daily for 14 days to induce stress similar to adverse childhood experiences. On the fifteenth day, stressed and non-stressed rats were either subjected to a concussion-like head injury under anesthesia or no head injury at all. The three conditions - stress alone, head injury alone, and combined stress with head injury - were compared to uninjured, non-stressed rats.

Examining the gene expression changes in the hippocampal region of the rats' brains during the juvenile period, the researchers found that stress alone and stress combined with traumatic brain injury induced notable effects. Both conditions activated pathways related to brain plasticity in excitatory and inhibitory neurons, suggesting a potential period of vulnerability or active changes in brain development.

Furthermore, both stress and combined stress-head injury conditions influenced oxytocin signaling, a hormone associated with maternal behavior and social bonding. While both stress conditions activated this pathway, brain injury alone inhibited it. This difference highlights the modulating effect of stress on how traumatic brain injury impacts the brain.

In behavioral tests conducted on adult rats, only those subjected to early-life stress displayed a tendency to enter wide-open spaces more frequently, a behavior that indicates a perceived vulnerability to predators. This aligns with human data that suggests early-life stress increases the risk of conditions such as ADHD and substance use disorders characterized by risk-taking behavior.

The researchers believe that these findings further emphasize the importance of addressing adverse childhood experiences. They suggest that social support and enrichment can serve as buffers against the detrimental effects of early-life stress, both in animal models and in humans.

The study was presented at the annual meeting of the Society for Neuroscience, Neuroscience 2023.

This study was made possible with the support of Ohio State's Chronic Brain Injury Institute, the Brain Injury Association of America, and a National Science Foundation Graduate Research Fellowship. The implications of this research can contribute to advancing our understanding of the impact of early-life stress and traumatic brain injury, leading to improved intervention strategies.