FLIPPING ROLE OF AMYGDALA IN MATURING BRAIN
In contrast to evidence
that the amygdala stimulates stress responses in adults, researchers at Yerkes
National Primate Research Center, Emory University have found that the amygdala
has an inhibitory effect on stress hormones during the early development of
nonhuman primates.
The results are published this week in Journal of
Neuroscience.
The amygdala is a
region of the brain known to be important for responses to threatening
situations and learning about threats. Alterations in the amygdala have been
reported in psychiatric disorders such as depression, anxiety disorders like
PTSD, schizophrenia and autism spectrum disorder. However, much of what is
known about the amygdala comes from research on adults.
"Our findings fit
into an emerging theme in neuroscience research: that during childhood, there
is a switch in amygdala function and connectivity with other brain regions,
particularly the prefrontal cortex," says Mar Sanchez, PhD, neuroscience
researcher at Yerkes and associate professor of psychiatry and behavioral
sciences at Emory University School of Medicine. The first author of the paper
is postdoctoral fellow Jessica Raper, PhD.
The findings are part
of a larger longitudinal study at Yerkes National Primate Research Center,
examining how amygdala damage within the first month of life affects the
development of social and emotional behaviors and neuroendocrine systems in
rhesus monkeys from infancy through adulthood. The laboratories of Sanchez and Yerkes
researchers Jocelyne Bachevalier, PhD and Kim Wallen, PhD are collaborating on
this project.
Previous
investigations at Yerkes found that as infants, monkeys with amygdala damage
showed higher levels of the stress hormone cortisol. This surprising result
contrasted with previous research on adults, which showed that amygdala damage
results in lower levels of cortisol.
The team hypothesized
that damage to the amygdala generated changes in the HPA axis: a network of
endocrine interactions between the hypothalamus within the brain, the pituitary
and the adrenal glands, critical for reactions to stress.
"We wanted to
examine whether the alterations in stress hormones seen during infancy
persisted, and what brain changes were responsible for them," Sanchez says.
"In studies of adults, the amygdala and its connections are fully formed
at the time of the manipulation, but here neither the amygdala or its
connections were fully matured when the damage occurred."
In the current paper,
the authors demonstrated that in contrast with adult animals with amygdala
damage, juvenile monkeys with early amygdala damage had increased levels of
cortisol in the blood, compared to controls. In their cerebrospinal fluid, they
also had elevated levels of corticotropin releasing factor (CRF), the
neuropeptide that initiates the stress response in the brain. Elevated CRF and
cortisol are linked to anxiety and emotional dysregulation in patients with
mood disorders.
Despite the increased
levels of stress hormones, monkeys with early amygdala damage exhibit a blunted
emotional reactivity to threats, including decreased fear and aggression, and
reduced anxiety in response to stress. Still, monkeys with neonatal amygdala
damage remain competent in interacting with others in their large social
groups. These findings are consistent with reports of human patients with
damage to the amygdala, Raper says.
"We speculate
that the rich social environment provided to the monkeys promotes compensatory
mechanisms in cortical regions implicated in the regulation of social
behavior," she says. "But neonatal amygdala damage seems more
detrimental for the development of stress neuroendocrine circuits in other
areas of the brain."
The investigators plan
to follow the animals into adulthood to investigate the long-term effects of
early amygdala damage on stress hormones, behavior and physiological systems
possibly affected by chronically high cortisol levels, such as immune, growth
and reproductive functions.
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