‘Hub’ of fear memory formation identified in brain cellsSeptember 29th, 2008 - 4:49 pm ICT by IANS
Washington, Sep 29 (IANS) A protein required for embryonic development also plays a key role in solidifying fear memories in adult animal brains, according to scientists. An apparent “hub” for changes in the connections between brain cells, beta-catenin could be a potential target for drugs to enhance or interfere with memory formation.
The protein beta-catenin acts like a Velcro strap, fastening cells’ internal skeletons to proteins on their external membranes that connect them with other cells. In species ranging from flies to frogs to mice, it also can transmit early signals that separate an embryo into front and back or top and bottom.
During long-term memory formation, structural changes take place in the synapses - the connections between neurons (nerve cells) in the brain, said Kerry Ressler, associate professor of psychiatry and behavioural sciences at Emory University School of Medicine.
“We thought beta-catenin could be a hub for the changes that take place in the synapses during memory formation. But because beta-catenin is so important during development, we couldn’t take the standard approach of just knocking it out genetically,” he said.
Ressler and graduate student Kimberly Maguschak used a variety of approaches to probe beta-catenin’s role in fear memory formation, such as stabilising the protein with a pulse of the psychiatric drug lithium and injecting a virus that could remove the gene for beta-catenin from brain cells, according to Emory University press release.
If mice are electrically shocked just after they hear a certain tone, they gradually learn to fear that tone and they show that fear by freezing.
To test beta-catenin’s involvement in fear memory, Maguschak used a genetically engineered virus paired with mice that had the DNA around their beta-catenin genes modified.
Once a cell is infected, the virus deletes the beta-catenin gene so that the cell can’t make beta-catenin protein. She injected the virus into the amygdala, a part of the brain thought to be important for forming memories of emotionally charged events.
“We found that after beta-catenin is taken out, the mice can still learn to fear the shocks,” said Maguschak. “But two days later, their fear doesn’t seem to be retained because they spend half as much time freezing in response to the tone.”
Beta-catenin appears to be turned on in the amygdala and involved in signalling during the learning process, Maguschak said.
“However, after the process of moving memories from short-term to long-term is complete, beta-catenin doesn’t appear to be necessary anymore,” she notes. “Injecting the virus after that point has no effect on the ability of the mice to express their fear memory.”
Maguschak also found that lithium salts, when given to the mice before training, make them even more afraid of the tone two days later.
“Psychiatrists have used lithium to treat mania and bipolar disorder for decades, but how it works is not well-understood,” Ressler said.
The results are scheduled to appear in the October issue of Nature Neuroscience.
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