from, The Flavor of Memories by TIME
Like just about every one of my contemporaries, I still remember
exactly where I was and what I was doing when John F. Kennedy was shot.
It's so vivid, it's almost like watching a movie: I was home sick from
fifth grade, lying on the couch in the living room. My mother had a
talk-radio station playing. Suddenly a newscaster broke in with the
news that shots had been fired in Dallas and that the President had
been rushed to a hospital. Then a few minutes later came these precise
words, spoken in just the tone you would imagine: "Ladies and
gentlemen, the President is dead," followed immediately by funereal
music. My mother burst into tears, and I, profoundly embarrassed, fled
the room.
That scene, which I have replayed many times since
1963, perfectly illustrates two crucial facts that neurologists have
come to understand in the past few years about the workings of human
memory--facts that have important implications for the treatment of a
variety of mental disorders, from post-traumatic stress to
obsessive-compulsive disorder. The first is that, despite its
movie-like clarity, my memory of J.F.K.'s assassination is almost
certainly wrong in some details, and maybe even some significant ones.
That's because I'm not simply calling up the original memory laid down
in November 1963. I'm recalling the last time I thought about it. Each
time we retrieve and re-store a memory, it can be subtly altered by all
sorts of factors. What goes back into our brains is like the new
version of a text document, overwriting the old.
The second
fact: memory and emotion are intimately linked biochemically, with
hormones like adrenaline actively involved in forming the neurological
patterns we call memories. "Any kind of emotional experience will
create a stronger memory than otherwise would be created," says James
McGaugh, a neurobiologist at the University of California at Irvine.
"We remember our embarrassments, our failures, our fender benders."
On
the face of it, that doesn't seem especially surprising: we feel strong
emotion at important events, which are obviously more memorable than
ordinary moments. But the connection is much deeper than that and dates
back to our deepest evolutionary past. "The major purpose of memory,"
observes McGaugh, "is to predict the future." An animal that can
remember the significance of that large, nasty-looking thing with the
big teeth and sharp claws will survive longer and produce more
offspring.
What happens biochemically, says McGaugh, is that
when faced with an emotion-charged situation, such as a threat, our
bodies release the stress hormones adrenaline and cortisol. Among other
things, these signal the amygdala, a tiny, neuron-rich structure
nestled inside the brain's medial temporal lobes, which responds by
releasing another hormone, called norepinephrine. Norepinephrine does
two important things. First, it kicks the body's autonomic nervous
system into overdrive: the heart beats faster, respiration quickens,
and the muscles tense in anticipation of a burst of physical exertion.
Second,
even as it's kick-starting the body, the amygdala sends out a crackle
of signals to the rest of the brain. Some of them put the senses on
high alert, ready to deal with a threat. But these signals also tell
the neurons that any memories recorded in the next few minutes need to
be especially robust. One piece of evidence for this scenario: Lawrence
Cahill, a colleague of McGaugh's at Irvine, showed subjects emotionally
arousing film clips, simultaneously gauging the activity of their
amygdalae using positron-emission tomography (PET) scans. Three weeks
later, he gave the subjects a surprise memory quiz. The amount of
amygdala activity predicted with great accuracy how well they
remembered the film clips.
Imaging studies also make clear that
it isn't just dangers or tragic events that cement memory formation.
Positive emotions, which are also mediated through the amygdala, have
the same effect. Again, that's a perfectly reasonable evolutionary
development. If eating or having sex makes you happy, you'll remember
that and do it again, keeping yourself healthy and passing on your
genes as well.
This is an oversimplification, of course. Other
neurotransmitters, and even plain glucose--the sugar the brain uses for
energy--may also play a part. And then there's the peculiar case of a
woman who contacted McGaugh because she remembers absolutely
everything. The stress-hormone model does not appear to apply in her
case. Says McGaugh: "At one point I asked if she knew who Bing Crosby
was. She's 40, so Bing Crosby doesn't loom large in her life, but she
knew he died on a golf course in Spain, and she gave me the date, just
like that." Imaging researchers are working to determine whether the
woman's brain is structurally different from everyone else's.
But
aside from such odd cases, virtually no expert doubts the connection
between the hormones of emotion and memory--and nobody doubts that
memory can be enhanced artificially. It's not necessarily a good idea,
though. Give someone a shot of adrenaline, and memory temporarily
improves. But it also drives up the heart rate, so it could be
dangerous for the elderly. Other memory enhancers, like Ritalin or
amphetamines, used by college students to cram for exams, are highly
addictive. And some of the experimental drugs McGaugh is testing in
rats can cause seizures. Unfortunately, he says, for people with truly
serious memory problems, "existing drugs are not yet powerful enough or
nice enough."
For people haunted consciously or unconsciously by
painful memories, there may be hope. Roger Pitman, a professor of
psychiatry at Harvard medical school, is working to understand
post-traumatic stress disorder (PTSD). The syndrome, he believes, is
the result of brain chemicals reinforcing themselves in a cerebral
vicious circle. "In the aftermath of a traumatic event," he says, "you
tend to think more about it, and the more you think about it, the more
likely you are to release further stress hormones, and the more likely
they are to act to make the memory of that event even stronger."
That's
consistent with McGaugh's ideas, but there are only a few bits of hard
evidence so far to support it. One bit comes from Israel: researchers
found that of people who showed up at emergency rooms after traumatic
events, those admitted with the fastest heartbeats had the highest risk
of later developing PTSD. Another is the surprising fact that after an
accident there's a much higher rate of PTSD in those with paraplegia
(paralysis of the lower body) than in those who suffer quadriplegia
(paralysis of all four limbs). "It doesn't make any psychological
sense," says Pitman. But it makes physiological sense because
quadriplegia severs the link between the brain and the adrenal glands.
To
test his theory, Pitman went to the the emergency room at Massachusetts
General Hospital in Boston and intercepted patients who had suffered
serious traumas. He gave some of them propranolol, a drug that
interferes with adrenaline uptake. The rest got placebos. He also had
them tape-record accounts of the traumas. When he played back the tapes
eight months later, eight of 14 placebo patients developed higher heart
rates, sweaty palms and other signs of PTSD. None of the patients on
the real drug had such responses.
Encouraged by his results,
Pitman is entering the third year of a much larger trial--one that has
stirred some controversy. The President's Council on Bioethics recently
condemned his study as unethical, saying that erasing memories risks
undermining a person's true identity. Pitman rejects such notions as a
bias against psychiatry. After all, he says, no one suggests that
doctors should withhold morphine from people in acute pain on the
grounds it might take away part of the experience.
Other
researchers are looking at PTSD as well. Michael Davis, a professor of
psychiatry at Emory University in Atlanta, is about to launch a study
of at least 120 soldiers returning from Iraq to see whether a compound
called D-cycloserine could help prevent PTSD. This compound activates a
protein that helps the mind form new, less emotional associations with
the original trauma, letting patients tolerate the memory better.
Studies in rats and humans have shown that it can work--and, says
Davis, "psychologists are very excited by it."
That's because
the theory behind D-cycloserine's action is totally consistent with
old-fashioned talk therapy, and especially with cognitive behavioral
therapy (CBT), currently the most effective nondrug technique dealing
with phobias, PTSD and obsessive-compulsive disorder. The idea behind
CBT--which first appeared in the 1950s, long before neuroscience could
explain such things--is that the patient examines upsetting ideas and
consciously assigns new, more positive associations to them. Even
old-fashioned Freudian psychotherapy might fit in with this model. By
dredging up forgotten memories, it may achieve the same thing, albeit
in a much less efficient way.
Medications like
D-cycloserine may simply streamline the process. Indeed, says Davis, at
least one study showed patients on D-cycloserine getting as much
benefit in two sessions as would normally take about eight. "That's
exactly what they're finding in obsessive-compulsive trials too," he
says. There are, moreover, a number of other brain receptors and
chemicals that show promise in accelerating the formation of new
associations. Says Davis: "People are now working on different targets
because we know so little about the process. What we have now could be
the tip of the iceberg."
And that's hardly surprising. Even
without anything approaching a complete understanding of the
complexities of the human brain, neurologists and psychopharmacologists
have come up with dozens of medications to treat schizophrenia,
depression and other disorders. The next batch of psychoactive drugs
could provide ammunition against the even more mysterious disorders of
memory.
With reporting by
Reported by Dan Cray / Los Angeles
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