Childhood Trauma Rewires the Brain in Ways That Fuel Both Aggression and Self-Harm

Researchers identify a neural pathway connecting trauma, pain, and destructive behavior.

A single neural thread in the brain may explain why some people who are hurt lash out while others turn the pain inward.

A new study published in Science Advances reveals that early-life trauma can rewire a key neural pathway connecting the thalamus and hippocampus, heightening pain sensitivity and triggering impulsive aggression or self-injury later in life. Researchers at the Fralin Biomedical Research Institute at Virginia Tech have mapped, for the first time, how overactive calcium channels in a small brain hub called the nucleus reuniens can set the stage for both destructive behaviors.

“Our findings suggest that aggression and self-harm may appear to be very different behaviors, but actually, they could share a common neural basis,” said Sora Shin, lead author of the study and assistant professor at Virginia Tech. “Both may exist along a continuum rooted in how the brain processes pain signals.”

The Pain Circuit Within

The thalamo-hippocampal circuit is a pathway linking the nucleus reuniens (RE) and ventral hippocampus (vCA1), which acts as a control center for how the brain interprets pain and emotion. When early trauma occurs, these neurons become oversensitive through changes in L-type calcium channels. These are molecular gates that regulate how brain cells respond to stimuli, the new study found.

In experiments with mice, activating these channels caused different reactions depending on dosage. At low doses, mice grew more aggressive, attacking cage mates faster and longer. At higher doses, they turned their teeth on themselves, biting their own paws and shoulders despite the availability of chew toys. But both reactions were accompanied by visible signs of distress.

“It’s changed the brain and molecular properties and caused hyperactivation of the neuron,” Shin said. “Excessive activity in that circuit increases susceptibility to aggression and self-harm.”

Mice given the calcium-channel stimulant showed facial grimaces — tightened eyes, flattened ears, twitching whiskers — and emitted distress squeaks. When given painkillers, the self-biting stopped.

From Childhood Trauma to Adult Behavior

To test how trauma alters this circuit over time, Shin’s team used a model of early-life stress. Mouse pups were separated from their mothers and observed. As adults, those mice became quicker to attack and more prone to self-harm after mild stimulation. Their brain scans showed elevated activity in the nucleus reuniens, and their neurons produced unusually high levels of the calcium channel gene Cacna1c. This molecular signature is also associated with anxiety and mood disorders in humans.

When researchers blocked those channels with the drug nicardipine, the violent and self-destructive behaviors subsided. Deleting the same gene in the nucleus reuniens had a similar calming effect.

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In essence, the findings suggest, trauma had left a fingerprint on the brain’s electrical circuitry — one that merged pain, fear, and impulse into a single feedback loop.

The researchers liken the nucleus reuniens to a decision hub that routes pain signals in two different directions. One set of its neurons connects to the hypothalamus, fueling aggression. Another set links to the amygdala, driving self-harm. Both stem from the same overstimulated channel network.

This may explain why people with trauma histories often oscillate between harming themselves and lashing out at others. “Aggression and self-harm are maladaptive coping strategies that often occur in individuals with a history of early-life trauma,” the researchers wrote in the study. “Excessive calcium channel activity in the nucleus reuniens increases the risk of both behaviors by altering pain processing and emotional regulation.”

A New Target for Treatment

The findings bridge a long-standing gap between psychology and biology. Clinicians have known that trauma survivors are more likely to engage in both self-injury and aggression, but the link was thought to be purely emotional and psychological. Shin’s research gives that link a physical address in the brain.

“Self-harm is also a pressing concern across many clinical populations,” she said. “Our study provides more open, active insights about the neural circuit basis that underlies these outcomes and may ultimately guide the development of more effective therapies.”

For now, the experiments remain in mice. But the identification of calcium channels as a potential lever opens new therapeutic directions. Think of drugs that can dial down the hyperactivity in this circuit without dulling the entire nervous system.