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 Research & Giving News Article  A team from Cold Spring Harbor Laboratory in New York and the Johns Hopkins University School of Medicine in Baltimore has found that surges of the stress hormone norepinephrine (also known as noradrenaline) that often accompany strong emotions spark a series of molecular events that ultimately strengthen the connections between neurons. The team, led by Dr. Roberto Malinow and which includes 2006 NARSAD Young Investigator Eleanore Real, Ph.D., reported their findings in the October 5, 2007, issue of the journal Cell. Where Were You On … 9/10? “This phenomenon is something everyone can identify with,” said Dr. Malinow, of Cold Spring Harbor Laboratory. “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.” Parts of the brain where memories are stored need to distinguish between significant experiences and those that carry less importance, the researchers explained. One factor critical in that process is the emotional load of an event. Studies have shown that heightened states of emotion can facilitate learning and memory. In some situations, the process can become pathological, Dr. Malinow pointed out. One instance would be post-traumatic stress disorder (PTSD), a condition characterized by persistent vivid memories of traumatic events. Stress Hormones Play a Part The stress hormone norepinephrine was previously known to play a central role in the emotional control of memory through its effect on receptors in the brain. During emotional arousal, the stress hormone is released by neurons that project widely to many brain regions, including the hippocampus and the amygdala, which are involved in the formation of emotional memory. Brain stimulation by norepinephrine had also been found to induce a phenomenon known as long-term potentiation (LTP). LTP involves a lasting increase in the strength of nerve connections, or synapses. That process is considered to be the cellular basis for learning and memory. “There were all these potential ways in which excitability or transmission might be enhanced by norepinephrine,” said Dr. Malinow. Yet, exactly how the stress hormone influences the processes involved in memory formation remained mysterious. A Key Receptor Strengthens Connections One way to strengthen synapses is to increase the number of so-called GluR1 receptors on the surface of neurons. Dr. Malinow’s group has shown that norepinephrine can do just that. In studies of mice, they revealed that norepinephrine, as well as emotional stress, leads to changes in GluR1 receptors at sites that play an important role in their delivery to nerve synapses. This chemical modification is both “necessary and sufficient” to lower the threshold for the receptors’ incorporation during LTP, thereby boosting memory, they showed. In behavioral tests of the animals, the group found that norepinephrine exposure can make normal mice remember events more clearly. By contrast, mice carrying mutations in their GluR1 receptors, specifically at the sites where modifications would be added, didn’t respond to norepinephrine with sharper recall. The brains of mice have “all the same parts” found in the human brain, Dr. Malinow said, and tests of emotional memory in people have shown that blocking the receptors for norepinephrine reduces the effects of emotion on learning and memory. “We expect that the molecular mechanisms are the same, as well,” he said. He emphasized, however, that the current study is just one piece of a much larger puzzle of how emotion influences memory. It remains unclear whether the newly identified mechanism plays a direct role in conditions such as PTSD. Nonetheless, Dr. Malinow 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.” This article was adapted by NARSAD with permission of Cell Press. |
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