Scientists Shed New Light on How Bad Experiences Change the Brain to Produce Memories


We know that everyday events can be easy to forget, but dangerous experiences that trigger fear can remain engraved in the brain for years. Now, scientists from NYU and Japan’s RIKEN Brain Science Institute have added to our understanding how this occurs.

Scientists Shed New Light on How Bad Experiences Change the Brain to Produce Memories
We know that everyday events can be easy to forget, but dangerous experiences that trigger fear can remain engraved in the brain for years. Now, scientists from NYU and Japan’s RIKEN Brain Science Institute have added to our understanding how this occurs. ©iStockPhoto/agsandrew

We know that everyday events can be easy to forget, but dangerous experiences that trigger fear can remain engraved in the brain for years. Now, scientists from New York University and Japan’s RIKEN Brain Science Institute have added to our understanding how this occurs.

In a study that appears in the latest edition of Proceedings of the National Academy of Sciences (PNAS), they identify the brain mechanisms responsible of translating unpleasant experiences into long-lasting memories that are critical for survival. This is achieved, they find, by changing the strength by which neurons are connected in the amygdala—the part of the brain involved in the formation of emotional memories.

The research tests a long-standing hypothesis on how the brain forms memories. Specifically, the findings show that this hypothesis, called Hebbian plasticity, partially explains memory formation. But the participation of other brain components is also required to remember new emotionally salient experiences.

“The convergence in the brain of weak and strong inputs--like the sight of a dog as it bites your leg--is sufficient to produce an association between the stimuli, but other mechanisms in the brain juice up the memory,” explains Joseph LeDoux, a professor in NYU’s Center for Neural Science and the director of the study.

The study, which also included Joshua Johansen, who directs the RIKEN Brain Science Institute’s Laboratory for Neural Circuitry of Memory, and Lorenzo Diaz-Mataix, a post-doctoral fellow in NYU’s Center for Neural Science, tested an influential theory proposed in 1949 by the Canadian psychologist Donald Hebb. Hebb’s theory posits that neurons that are connected and fire electrical impulses at the same time increase the strength of their connections and, by doing so, lay the basis for memory formation.

A great deal of work in reduced brain preparations has demonstrated that this type of Hebbian plasticity can indeed increase the connectional strength between neurons. However, this idea of Hebbian plasticity remained untested in the working brain for actual memory formation in the complex brains of mammals. So the question remained: does direct electrical excitation of amygdala neurons by aversive experiences trigger aversive memory formation?

In the PNAS study, the authors were able to electrically silence electrical activity during the shock period in experiments on threat conditioning. In these experiments, a neutral auditory tone is paired with a mild electrical shock to create emotional reactions.

They found that preventing the electrical activity resulted in impaired memory for the aversive event that was reflected in the lack of learning induced strengthening of the connections between neurons in the amygdala. This finding provided direct support for the Hebbian hypothesis.

“Fifty years before Hebb, neuroscientist Santiago Ramón y Cajal, merely observing the brain with very rudimentary microscopes, already suggested the basic Hebbian hypothesis,” explains Diaz-Mataix. “Now, 100 years later, using today’s technologies, we can say that he was right.”

However, when they eliminated the shock and replaced it by pairing the auditory stimulus with direct laser excitation of the amygdala cells, no learning occurred. Surprisingly, learning did occur when the receptors for noradrenaline, a brain molecule that is important for attention, were activated at the same time as the laser was on. This demonstrates that while Hebbian mechanisms are important, they are not sufficient by themselves. Rather, the participation of tiny molecules called neuromodulators seem to be required.

“This takes us a step closer to understanding how aversive experiences are translated by the nervous system into unpleasant memories,” Johansen explains. “These processes for triggering aversive memory storage may represent a general mechanism controlling memory formation that is shared across other learning systems in the brain.”

“Understanding how aversive memories are formed is particularly relevant to anxiety disorders, such as in post-traumatic stress, in which chemicals like norepinephrine are known to contribute to hyperarousal and may imprint memories especially strongly,” LeDoux adds.
 

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