McGaugh and Cahill showed two groups of subjects 12 slides accompanied by a narrative. One group heard a neutral story about a mother and son visiting a hospital to watch a disaster drill. The second group heard the same story, but with a grisly embellishment: The boy had been struck by a car, and doctors had to reattach his severed feet. Two weeks later, those who had heard the emotionally arousing story had much better recall of the narrative’s details, presumably because a jolt of epinephrine to their amygdalas had heightened their memory of it.
Next, McGaugh and Cahill tested a new group of subjects. But this time, half of those who were to see the slides and hear the disturbing narrative first received an injection of propranolol, while half got a placebo shot. Two weeks later, the placebo group had excellent recall of the stimulating part of the story, but those who had taken propranolol had no better memory of the entire story than did those who had heard the dull version.
The drug keeps adrenaline from activating beta-adrenergic receptors in the amygdala, and in this case, that apparently prevented the enhancement of an emotional memory. “For the first time, we proved it was possible to stop the formation of strong memory in humans by blocking the action of a hormone released by emotional arousal,” says McGaugh. The following year, when Cahill repeated the experiment on a German subject who was missing his amygdala because of disease, the man’s recollection of the exciting story was just as bland as the memories of those who had received propranolol—further evidence that the amygdala modulates the strength of an emotional memory.
Timing, however, is crucial in loosening memory’s grip. In order for new learning or the memory of an experience to be stored, nerve cells (neurons) must transmit information from one to the next, crossing junctions called synapses. And while communication within a neuron is conducted electrically, the information carried between neurons, across the synapses, normally travels via chemicals (neurotransmitters). When learning occurs, that chemical communication is enhanced, usually because an increased number of receptors have formed on neurons to process the neurotransmitters.
Learning then becomes fixed as a long-term memory. For that to happen, neurons synthesize proteins that generate new receptors and stimulate the growth of synapses—strengthening the communication network between neurons and enhancing the transmission of neurotransmitters. This process of creating permanent structural changes in the brain is called memory consolidation, and it’s estimated to take from a few minutes to a few hours. That leaves only a brief window to interfere with a traumatic memory before it becomes permanent.
The amygdala stores the emotional, unconscious component of a memory, while conscious memory resides in the nearby hippocampus, although scientists suspect the hippocampus may be only a way station, holding the memory temporarily before transferring it to other brain regions for permanent storage. Recall a strong memory, and your amygdala will cause your body to react—setting your heart racing, for example—at the same time your hippocampus releases explicit details. And even though two brain regions are reading out data independently, we perceive our memories as seamless.
In 2002, operating under the time constraint that memory consolidation imposes, emergency room nurses at the Massachusetts General Hospital (MGH) recruited trauma victims to participate in a research trial to determine whether propranolol could prevent PTSD. Eventually 41 people agreed, and each received either a placebo or propranolol four times a day for 10 days and then a reduced dose for another nine days. The subjects also wrote accounts of their traumas, which ranged from rape to auto accidents, and researchers summarized and read the reports into a tape recorder. Three months later, as subjects listened to their taped stories, 43% of the placebo group experienced racing hearts, sweaty palms and twitching muscles. But none of the subjects who had taken propranolol showed a strong physical reaction when revisiting the trauma. Yet when asked whether traumatic memories were affecting their lives, both groups offered the same range of responses. In both groups, some people remained very troubled, while others seemed little affected.
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