Depressed mice recover with molecular therapy
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Depressed loner mice get more sociable when researchers delete a memory molecule from their brains, a finding that might help treat human ills like social phobia and post-traumatic stress, scientists said on Thursday.
This molecular therapy worked about as well as giving mice the antidepressants Prozac or Tofranil, the researchers reported in the current issue of the journal Science.
They targeted a molecule in a section of the brain known to be related to sensations of pleasure and danger, said Olivier Berton of the University of Texas Southwestern Medical Center, one of the report’s authors.
“We focused on this molecule in a region of the brain that people call the reward pathway, which people have studied a lot in relation to drugs that are abused,” Berton said in a telephone interview.
Deleting the molecule from this part of the brain meant that the mice never got depressed and fearful, Berton said, even though conditions were set up that normally would make them run away and hide.
“If we can identify such mechanisms in the brain, that’s a way to develop antidepressants that work faster and in more people,” Berton said.
To carry out the experiment, Berton and his colleagues had to find a way to reliably make mice depressed. They did this by putting ordinarily sociable mice in cages with aggressive, bullying mice.
The sociable mice regularly fought with the bullies, and over a period of days became withdrawn and fearful of strange mice. Even when the bullies were removed, the depression stayed.
They perked up when dosed with antidepressants for a month, Berton said.
Deleting the molecule involved anesthetizing the mice, then injecting this very specific part of their brains with a virus that disabled the molecule. This kind of technique has been used experimentally in research into Parkinson’s disease, Berton said.
The result in mice was to block the typically depressed response to bullying, mimicking the response to chronic antidepressant therapy.
The next step is to record the electrical activity of brain cells in the reward pathway, Berton said in a statement released by his university.
“We’re trying to understand this response to stress from the molecular to the cellular to the neural circuit level of understanding,” he said.
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