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Discovering Our Selves: The Science of Emotion
Executive Summary

Panel: The Science of Memory and Emotion

"How Emotions Strengthen Memory"

James L. McGaugh, Ph.D., is Research Professor of Psychobiology at the University of California-Irvine and founder and Director of the Center for the Neurobiology of Learning and Memory.

From both human and animal studies, we know that a certain class of anxiety-reducing drugs called benzodiazepines (Valium and Halcion, for example) impair memory consolidation. Other classes of drugs have the opposite effect and can enhance memory, but only if they are administered shortly after learning, when memory consolidation is occurring. If the injections occur more than six hours after training, memory is not enhanced.

Both kinds of drugs work on the same receptors in the basolateral nucleus of the amygdala, receptors for the inhibitory neurotransmitter GABA, which blocks the firing of the receiving neuron or moderates the strength of its firing. The amnesia-inducing drugs are GABA agonists: they act like GABA itself to activate the GABA receptors. The memory enhancing drugs are GABA antagonists: they block activation of the GABA receptors.

Memory also is enhanced by hormones that are released when we experience stress. This explains why emotional arousal has such a powerful influence on how well we remember things. When the brain senses danger, the instant fight-or-flight response involves the hypothalamus sending signals along the sympathetic nervous system to the adrenal glands, specifically to the adrenal medulla, which secrete the hormones epinephrine (also called adrenaline) and norepinephrine into the blood stream. Adrenaline raises the heart rate; norepinephrine raises blood pressure.

If the threat continues for more than a few seconds, the HPA (hypothalamus-pituitary-adrenal) axis is activated. The hypothalamus releases a hormone called CRH (corticotropin releasing hormone), which stimulates the pituitary gland to secrete ACTH (adrenocorticotropic hormone), which in turn stimulates the outer part of the adrenal glands, the adrenal cortex, to produce cortisol. Cortisol, among other things, increases the supply of blood glucose to make more energy available, enabling the fight and/or the flight. Both epinephrine and cortisol play a very powerful role in regulating the strength of memory by regulating the release of norepinephrine in the basolateral nucleus of the amygdala.

Even though the amygdala is crucial to the consolidation of emotional memories, it is not the site of long-term storage of the memories. Animal studies show that when animals are trained with mild foot shocks (a sufficiently negative experience to induce the stress response) and then have their amygdalas inactivated by injections of lidocaine, they can still perform the training task; their memory is not affected.

We know from human experiments that the strength of a memory is regulated by the significance of the experience. The regulation involves the release of stress hormones. In one experiment, two groups of subjects were read a story and shown a series of slides. They all saw the same slides, but they heard two different stories. One story was flat and neutral; the other story matched it except for an emotionally arousing description in the middle.

Two weeks later, the subjects were asked to state what they remembered of the slides. The group that heard the neutral story remembered the slides from all parts of the story equally well (or poorly); there was no difference in recall of the slides from the beginning, middle, or end of the story. The other group, however, had significantly enhanced recall of the slides in the middle, the ones they were looking at when they heard the emotionally arousing description.

In a subsequent experiment, half the subjects were given a beta blocker (to block epinephrine effects) before the experiment started. For those who heard the neutral story, the beta blocker made no difference in their recall of the slides. But in those who heard the emotional story, the beta blocker completely blocked the arousing effect of emotion on memory, preventing the memory from becoming strong.

These results have clear implications for people who are plagued by vivid memories of a trauma and are suffering from post-traumatic stress disorder. It may be possible to block the development of post-traumatic stress disorder by artificially--that is, pharmaceutically--blocking the effects of stress hormones in the brain. If we can reduce the emotional charge of the memory of an assault or an accident, we can reduce the long-term anxiety.

When the connection between emotion and memory works well, the results are very satisfying: we remember the important and good things that we want and need to remember. When the system is overworked, we may remember too much, or too intensely, and the result may be debilitating.


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