Mice that witnessed other rodents developed depression, according to a new study


New research from Japan suggests that mice are empathetic and can become depressed just by watching other rodents being bullied.

A team from Tokyo University of Science believes that exposure to vicarious stress leads to the deterioration of neurons in the hippocampus, which they see as a key factor in depression.

This so-called “second-hand” depression could shed light on how people develop mental health problems and how they are treated, the scientists said.

“I want people to think about how stress can change not only the brains of people with depression, but also our brains – those who watch it -” lead author Akiyoshi Saitoh, professor of pharmacology, told Vice.

Mice made to watch other rodents being bullied developed symptoms of depression, including social withdrawal and inability to enjoy joy

The researchers decided to study how stress affects neurogenesis in the hippocampus, a small but complex brain structure that sits on the underside of each temporal lobe and is associated with learning, emotions, and memory.

“We decided to focus on the possible mechanism of mental stress involved in hippocampal neurogenesis in adults in order to understand its role in depressive disorders,” Saitoh said in a press release.

Neurogenesis is the process by which new neurons are formed in the brain.

Research by Saitoh and his colleague exposed mice to “chronic vicarious social failure stress” by repeatedly watching another mouse become overwhelmed.

They put two mice in a cage, one larger than the other, and pushed the smaller one into the territory of the larger rodent.

In the brains of the spectator mice, new neurons had a reduced survival rate in the dentate gyrus, a region of the hippocampus related to memory and sensory perception. The authors believe that deterioration was a major contributor to their depression

The larger mouse would be aggressively defending its space, but it wasn’t the smaller mouse the team was interested in: it was a third mouse, safely sitting in its own cage, watching the whole ordeal.

Although there was no risk, the spectator mice developed depressive symptoms.

After 10 days, they showed signs of anhedonia or an inability to experience pleasure – a key symptom of depression in humans.

“If you give mice a choice to drink plain or sweet water, they’ll almost always drink the sweet drink because it’s more comfortable,” Saitoh told Vice. “But the mouse that witnessed social defeat did not, which indicated a decreased need for pleasure,” he said.

The study was recently published in the journal Behavioral Brain Research.

Saitoh described the Witnesses as “almost like Hikikomori,” young adults in Japan who are so withdrawn into their parents’ homes that they cannot work or go to school.

“They weren’t interested in other mice, which is unusual because mice are social beings,” he said.

There was also a physiological change: new neurons in the spectator mice had reduced survival in the dentate gyrus, a region of the hippocampus related to memory and sensory perception.

The authors believe that deterioration was a major contributor to their depression.

Neuron survival rates recovered after viewers were given the antidepressant fluoxetine, the selective serotonin reuptake inhibitor commonly known as Prozac.

But they “didn’t make sudden, full recoveries,” Saitoh said. In fact, the symptoms returned a few weeks later.

That’s important to understand that treating depression in humans isn’t a quick fix, he added.

Co-author Toshinori Yoshioka said in the press release that the team believes the experiment “will play an important role in elucidating the pathophysiology of depression and in developing a novel drug related to it.”

The dentate gyrus is one of the few brain organs where neuron growth continues into adulthood in many mammals, including mice and primates.

But while some studies suggest that neurogenesis in the human dentate gyrus persists for a lifetime – even into the 1970s – others say it drops to undetectable levels in adults after childhood.

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