New clues to why stressful memories remain so vivid
From NSERC BULLETIN - #182
(Ottawa) - One of the more fascinating findings in experimental psychology is the existence of a neurochemical basis for the mutability of memory.
According to this understanding, a memory, once consolidated after initial learning, is not hardwired for all time. Opening it triggers a process of rewiring or “reconsolidation” that creates a new memory that may not be exactly the same as the original. For psychologists, this has suggested the tantalizing possibility of softening harsh memories and treating the ravages of diseases such as Post Traumatic Stress Disorder (PTSD).
However, nothing is simple about brain functioning.
“Reconsolidation may be a fundamental process in many species,” said McGill psychologist and 2009 NSERC E.W.R Steacie Memorial Fellow Karim Nader, “but we also know that not all memories seem to undergo reconsolidation. For example, very strong memories, such as that of a fear of noise, don’t seem to reconsolidate, two, or even seven, days after training. However, they do resume reconsolidating after a month or two.”
“It’s not hard to guess why these short term memories should remain so fixed,” he said. “There would be an obvious survival advantage for an animal to keep a robust memory of an incident that scared it.”
Exactly how the brain determines which memories undergo reconsolidation and which factors control the process were the major focus of a recently-published international study that involved Dr. Nader.
The researchers zeroed in on a receptor molecule called NMDA that Dr. Nader and a colleague had previously found to be critical for learning, and to transforming memory that is fixed in the brain to an unstable, unwired memory.
“NMDA has to be activated in order for a memory to become unwired,” he said. “The memory can still be remembered, however.”
In the study, the researchers followed NMDA workings in the brains of two different groups of laboratory rats. One had been given strong aversive auditory training; the other, weak training.
“We found reduced levels of NMDA when the strong memories were not undergoing reconsolidation, several days after the stress event, but the levels return to normal levels later when the reconsolidation process resumed,” he said.
“So the NMDA receptors act like a switch. When levels are low, they say that this memory should not undergo reconsolidation and remain wired into your brain.”
"There was also," he added, "evidence for the involvement of another brain area separate from where the memory was stored."
The findings may have important clinical implications.
“If you want to treat Post Traumatic Stress Disorder by targeting reconsolidation, then you want to wait for a few months after the trauma,” he said. “Starting too soon may be fruitless."
This finding also aligned with a trend in the PTSD study that he was part of in 2008, where the individuals with older trauma were the best responders.
“Another possibility is that if we give people drugs that activate the NMDA receptor, it may trigger the memory to reconsolidate again.”
The paper “Cellular and systems mechanisms of memory strength as a constraint on auditory fear reconsolidation” was published on-line in Nature Neuroscience on June 21, 2008.