Really bad experiences, like going through a particularly stressful or frighting situation, are a lot easier to remember than the things we do a day to day basis, or even those special pleasant experiences. That’s because we’re sort of evolutionary geared to remember those particularly nasty experiences so that we might avoid these in the future. A collaborative effort between New York University and Japan’s RIKEN Brain Science Institute wanted to see what changes occur in the brain that facilitate this transfer of experience to memory. The team put to the test a hypothesis first posited in 1949 and found that it matches. Namely, the neuroscientists discovered than an increase of connection strength between neurons in the amygdala – the part of the brain involved in the formation of emotional memories – is the main driving factor. It’s not alone though, as other brain components needs to participate to remember new emotionally salient experiences.

Unpleasant memories stick when neuron activity intensifies

Unpleasant memories are a lot easier to form than regular ones. Image: Silence of the Lambs.

Unpleasant memories are a lot easier to form than regular ones. Image: Silence of the Lambs.

“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.

In 1949, Canadian psychologist Donald Hebb first proposed an influential theory that claimed 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. The claim, which remained in literature under the name of “Hebbian plasticity”, has been tested before with confirming results, but never  in the working brain for actual memory formation in the complex brains of mammals.

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To put the Hebbian plasticity hypothesis to its hardest test yet, LeDoux and colleagues staged a traumatic experience for mice. The mice would receive an electric shock, paired with a neutral auditory tone. This is a classic experiment, done many times before, where most of the time the mice remember the experience and become frightened when hearing the tone, but absent the actual shock. Memories can be just as petrifying as the actual event that caused the memory to be stored in the first place.

The researchers employed a nifty trick, though – they silenced the mouse brain’s electrical activity during the shocking event. They found that preventing the electrical activity resulted in impaired memory for the aversive event that was reflected in the lack of learning, typically induced by strengthening the connections between neurons in the amygdala.

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

A surprising find followed in a second experiment. When the electrical shock was replaced by a laser light shone directly into the amygdala target cells, no learning occurred. However, when  the receptors for noradrenaline, a brain molecule that is important for attention, were activated at the same time as the laser was on learning occurred. This tells us that while the Hebbian mechanism is valid, it does not work alone to store the bad memories.

“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.

While bad memories are easier to form, it’s interesting to hear about research that erases these. Last I year I had the pleasure of reporting a fascinating study in which researchers from the Scripps Research Institute (TSRI) eliminated dangerous drug-associated memories in mice and rats without apparently affecting other memories. I’m not saying it would be a good idea to try this with humans, but interesting nonetheless.

Findings appeared in the journal Proceedings of the National Academy of Sciences (PNAS).