February 2015 • Monitor on Psychology 45
it changes the strength of synaptic transmission and learning,”
says Huganir. “The trick is being able to selectively disrupt or
enhance these mechanisms in different regions of the brain.”
Other researchers are looking at whether lifestyle interventions,
such as exercise, might also influence how we process memories.
For example, brain-derived neurotrophic factor (BDNF) is
a naturally occurring protein that regulates the growth of
neurons and synapses. Lower blood levels of BDNF signal that a
patient may not respond well to exposure therapy, for reasons as
yet unclear. Although BDNF isn’t given as a drug, blood plasma
levels can be increased through moderate to intense physical
exercise, and a recent study showed that aerobic exercise
reduced PTSD symptoms, an area that needs more study
(Cognitive Behaviour Therapy, 2014).
“I don’t believe the effects of exercise — the timing and
amount of it, and how it affects mental health and treatment
for PTSD — have been adequately researched or manipulated,”
Other factors might include how soon a patient should
sleep after exposure therapy, as sleep plays a role in memory
“Sleep is key for learning, and people with PTSD show
reduced or disrupted sleep. Recent data show that extinction of
conditioned fear occurs more effectively in the morning versus
the evening, suggesting that there may be optimal times of the
day for exposure therapy,” Quirk says.
Timing exposure therapy to a woman’s menstrual cycle
could also enhance its benefits. A number of studies suggest
hormone levels may influence treatment effectiveness, and
there is evidence that estrogen activates parts of the brain
responsible for extinguishing conditioned fear. The work of
Mohammed Milad, PhD, at Massachusetts General Hospital
showed that women with lower estradiol levels had poorer
extinction recall than both women with higher levels and than
men (Neuroscience, 2010). The same group found that female
rats with higher levels of estrogen and progesterone were better
able to consolidate fear extinction; injecting the hormones also
facilitated extinction learning (Neuroscience, 2009).
Still, promising as they are, clinical applications of
physiological memory tinkering are likely many years away.
“It’s neat that these higher order processes can be
manipulated, but we do have to be cognizant of not
anthropomorphizing too much in this because there’s a lot in
humans we can’t model in animals,” Ramirez says.
As part of President Obama’s BRAIN Initiative — Brain
Research through Advancing Innovative Neurotechnologies —
scientists from various organizations will be further exploring
the cellular mechanisms of learning and memory over the next
Greater collaboration between neuroscientists and
psychologists in treating anxiety disorders can be expected as
“Talk therapies are really triggering neural circuits and
manipulating the brain, but if neuroscientists can understand
how that’s happening, we may be able to facilitate the therapy,”
Quirk says. n
• Milad, M. R., & Quirk, G. J. (2012). Fear Extinction
as a Model for Translational Neuroscience: Ten Years of
Progress. Annual Review of Psychology, 63, 129–151.
• Hofmann, S. G., Wu, J. Q., & Boettcher, H. (2013).
D-Cycloserine for Treating Anxiety Disorders: Making
Good Exposures Better and Bad Exposures Worse. Biology
of Mood & Anxiety Disorders, 3( 11).
• Milad, M. R., Rosenbaum, B. L., & Simon, N.
M. (2014). The Neuroscience of Fear Extinction.
Neuroscience, 62, 17–23.
• Hall, S. S. (2013, June 17) “Repairing Bad Memories,”
MIT Technology Review, 116( 4), 48–54.
“In years to come, neuroscience will inform clinical
practice. We will use both biological and neurological
measures to give us clues as to treatment.”
Stefan Hofmann, PhD