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The newspaper of The Johns Hopkins University October 8, 2007 | Vol. 37 No. 6
 
Scientists Discover What Emotional Memories Are Made Of

By Nick Zagorski
Johns Hopkins Medicine

Both extensive psychological research and personal experience confirm that events that happen during heightened states of emotion — such as fear, anger and joy — are far more memorable than less- dramatic occurrences. In a report in the Oct. 5 issue of Cell, Johns Hopkins researchers and their collaborators at Cold Spring Harbor and New York University have identified the likely biological basis for this: A hormone released during emotional arousal "primes" nerve cells to remember events by increasing their chemical sensitivity at sites where nerves rewire to form new memory circuits.

Describing the brain as a big circuit board in which each new experience creates a new circuit, Johns Hopkins neuroscience professor Richard Huganir said that he and his team found that during emotional peaks, the hormone norepinephrine dramatically sensitizes synapses — the site where nerve cells make an electro-chemical connection — to enhance the sculpting of a memory into the big board.

Norepinephrine, more widely known as a "fight-or-flight" hormone, energizes the process by adding phosphate molecules to a nerve cell receptor called GluR1. The phosphates help guide the receptors to insert themselves adjacent to a synapse. "Now when the brain needs to form a memory, the nerves have plenty of available receptors to quickly adjust the strength of the connection and lock that memory into place," Huganir said.

Huganir and his team suspected that GluR1 might be a target of norepinephrine because disruptions in this receptor cause spatial memory defects in mice. They tested the idea by either injecting healthy mice with adrenaline or exposing them to fox urine, both of which increase norepinephrine levels in the brain. Analyzing brain slices of the mice, the researchers saw increased phosphates on the GluR1 receptors and an increased ability of these receptors to be recruited to synapses.

When the researchers put mice in a cage, gave a mild shock, took them out of that cage and put them back in it the next day, mice who had received adrenaline or fox urine tended to "freeze" in fear — an indicator that they associated the cage as the site of a shock, more frequently, suggestive of enhanced memory.

However, in a similar experiment with mice genetically engineered to have a defective GluR1 receptor to which phosphates cannot attach, adrenaline injections had no effect on mouse memory, further evidence of the "priming" effect of the receptor in response to norepinephrine.

The researchers plan on continuing their work by going in the opposite direction and engineering another mouse strain that has a permanently phosphorylated or "primed" receptor. "We're curious to see how these mice will behave," Huganir said. "We suspect that they'll be pretty smart but at the same time, constantly anxious."

The research was funded by the National Institutes of Health, Howard Hughes Medical Institute, Damon Runyon Postdoctoral Fellowship, NARSAD, and Ale Davis and Maxine Harrison Foundation.

Authors on the paper are Hailan Hu, Eleonore Real and Roberto Malinow, all of Cold Spring Harbor Laboratory; Joe LeDoux, of New York University; and Kogo Takamiya, Myoung-Goo Kang and Huganir, all of Johns Hopkins.

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