Why Doesn’t a Dog’s Trauma Just Fade Away?

Does your dog still react with fear to something that happened long ago? Growl at a sound that reminds them of fireworks? Flinch at the sight of an object that merely looks like “that thing”? Science has just taken a significant step toward explaining why this happens.

New research from the Institute for Basic Science suggests that the problem with “letting go” of trauma — in both humans and dogs — may not lie in neurons alone, but in the brain’s support cells: astrocytes. It sounds like a small detail. It may turn out to be anything but. In fact, it could open the door to an entirely new way of thinking about PTSD.

The study was conducted in humans and mice, not dogs. But its implications are highly relevant to how we understand post-traumatic disorders in dogs as well. Dogs, like humans, can carry fear long after the original source is gone. And the standard tools — desensitization, counterconditioning, serotonin-based medication — do not always work. Perhaps because the problem sometimes lies deeper.

GABA, Fear, and the Failure to Let Go

PTSD is a condition in which the brain struggles to extinguish fear. Even when the danger has long passed, the body continues to react as if the trauma were still happening.

Until now, the main suspect was excessive neuronal activity. But this new study points elsewhere: to an excess of GABA, an inhibitory neurotransmitter, produced not by neurons but by astrocytes.

That matters because in this context, too much GABA does not simply calm the system down. It appears to interfere with the brain’s ability to extinguish fear. In particular, it disrupts processes in the medial prefrontal cortex, a region involved in emotional regulation and decision-making.

It is as if the brain’s regulatory system is trying to move forward with the handbrake still on.

Seen from that angle, post-traumatic behavior is not “disobedience,” not stubbornness, not a dog being dramatic. It is a neurochemical trap.

A New Drug?

The research team found that the excess GABA was linked to the activity of the MAOB enzyme — monoamine oxidase B — in astrocytes. They then developed a drug, KDS2010, designed to block this enzyme.

In mice showing PTSD-like symptoms, the results were striking: brain function in the medial prefrontal cortex normalized, anxiety-like symptoms decreased, and blood flow in that brain region improved.

Importantly, the drug has already passed phase I clinical trials in humans.

What About Benzodiazepines?

This finding also casts new light on a class of drugs often used in traumatized dogs: benzodiazepines.

These medications also work through GABA. And if excessive GABA may itself contribute to the persistence of trauma, then benzodiazepines may not always help the brain extinguish fear. In some cases, they may even make that process harder.

There has long been a suspicion that these drugs often mask symptoms rather than address the underlying mechanism. This research offers one possible explanation why. They may be reinforcing the very system that helps keep PTSD alive.

That does not mean they should never be used. But it is a strong argument for using them carefully, thoughtfully, and only when clearly justified.

What Does This Change in Work with Dogs?

First, it calls for more patience and less pressure. A traumatized dog may not be “holding on” to fear by choice. The brain may simply be unable to let go yet.

Second, it suggests that exposure alone is not enough. If trauma affects the dog’s ability to regulate, then recovery has to involve rebuilding regulation, not just confronting reminders of the original event.

Third, it adds another layer of caution around medication choices. In some cases, drugs that deepen GABA activity may not be helping in the way people hope.

And finally, it reminds us to stay open to new directions. Targeted MAOB-based therapies may one day become part of treatment. For now, the most effective work still lies in helping the dog regain emotional regulation and creating an environment that feels genuinely safe.

This study changes the frame. It suggests that the cells supporting the brain — not just the neurons themselves — may be helping to maintain trauma.

And that means the future of trauma treatment, in animals as well as humans, may look very different from what we assumed.

Perhaps the most important takeaway is this: a traumatized dog is not a problem to be fixed. It is a brain in crisis.

A brain that needs time, safety, support — and perhaps, one day, a new generation of treatment.

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Sujung Yoon et al, Astrocytic gamma-aminobutyric acid dysregulation as a therapeutic target for posttraumatic stress disorder, Signal Transduction and Targeted Therapy (2025). DOI: 10.1038/s41392-025-02317-5