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days became withdrawn and fearful of strange mice.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.

By Deborah Zabarenko

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