Washington, October 5 : Scientists have confirmed that events that happen during heightened states of emotion such as fear, anger and joy are far more memorable than less dramatic occurrences.

Writing about their study on mice in the journal Cell, a publication of Cell Press, the researchers have revealed that such an effect is down to surges of the stress hormone norepinephrine, which is released by neurons that project widely to many brain regions such as hippocampus and the amygdala, which are involved in the formation of emotional memory.

“This phenomenon is something everyone can identify with. You can probably remember where you were when you heard about 9/11, but you probably don’t know where you were on 9/10. We've identified one mechanism that may underlie this effect,” said Roberto Malinow of the Cold Spring Harbor Laboratory in New York.

The researchers say norepinephrine causes this effect by inducing a phenomenon called long-term potentiation (LTP), which involves a lasting increase in the strength of nerve connections, or synapses. This process is considered to be the cellular basis for learning and memory.

They have also revealed that norepinephrine strengthens synapses by increasing the number of GluR1 receptors at neurons’ receiving ends.

It was found during the study that norepinephrine, as well as emotional stress, lead to the addition of a chemical phosphate group to GluR1 receptors at sites that play an important role in their delivery to nerve synapses.

The study showed that chemical modification is both “necessary and sufficient” to lower the threshold for the receptors’ incorporation during LTP, and to boost memory thereby.

During the study, 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.

Malinow revealed that normal mice exposed to norepinephrine ended to “freeze” in fear when they were put back in the cage the next day, an indication that they remembered the event more clearly. On the other hand, mice with mutations in their GluR1 receptors, specifically at the sites where phosphates would be added, did not respond to norepinephrine with sharper recall.

Malinow said that the brains of mice have “all the same parts” found in the human brain, and that tests of emotional memory in people had shown that blocking the receptors for norepinephrine reduce the effects of emotion on learning and memory.

“We expect that the molecular mechanisms are the same, as well,” he said.

He admitted that current study was just a part of a much larger puzzle of how emotion influences memory, and that it had yet to be determined whether the newly identified mechanism played a direct role in conditions such as posttraumatic stress disorder (PTSD).

He, however, said, “we’ve identified one potential therapeutic target. It may be possible to develop drugs that could prevent too many brain receptors from being added or that might remove them once they are there.” (ANI)