Laboratory of Stress and Resilience
Faculty
Julie Fudge, MD
The amygdala is a major limbic structure that is involved in the emotional coding of
environmental stimuli. In particular, the amygdala is activated by threatening
or fearful stimuli in humans. In mood and anxiety disorders, the amygdala is
hyperactivated, suggesting aberrant ‘overcoding’ of negative stimuli. Our
work has shown that the amygdala is characterized by unique connections to the monoamine
systems. In particular, key output regions of the primate amygdala such as
the central nucleus are strongly innervated by the serotonin system, indicating a
major pathway for control of anxiety behaviors by serotonin enhancing drugs (SSRIs). These
same output paths have direct connections to the hypothalamic-pituitary-adrenal axis,
providing a way for emotionally relevant information in the external milieu to directly
affect the ‘stress axis’. Another line of research is to
characterize amygdala cell populations that have an immature phenotype. These
cells reside in the subventricular zone near the lateral horn of the ventricle in
primates, and contain a number of markers typical of immature neurons. They
are richly innervated by serotonin containing fiber, suggesting that serotonin plays
a role in their survival and growth. Our goal is to determine the distribution
and developmen
t
of these cells across the lifespan, and determine their responsiveness to treatment
interventions in primate models.
Dana Helmreich, PhD
My broad research emphasis is on the hormonal and behavioral sequelae of stress, and
how these outcomes may be altered by effective coping mechanisms, such as perceived
control and voluntary exercise. These active coping behaviors may promote
resilience in the presence of ongoing stressors. Currently my research, using
adult rats, is focused on changes that occur in hypothalamic neurons that control
both the hypothalamic-pituitary-adrenal axis and the hypothalamic-pituitary- thyroid
axis in animals that have the opportunity to perform active coping behaviors and
in animals in which these behaviors are prevented. Additionally, we are initiating
studies to determine how stress and coping alter amygdaloid neural circuits and associated
behavior.
David Parfitt, PhD 
One aim of our behavioral neuroendocrinology laboratory is to understand how early
life stressors alter brain mechanisms that ultimately alter physiology and behavior
long-term. We are currently developing a mouse model to explore the impact
of neonatal rearing environment on offsprings’ future susceptibility or resilience
towards future stressful situations. Our research laboratory utilizes a whole
animal approach with a variety of techniques to elucidate how early life stressors
alters behavior (maternal behavior towards the developing pups as well as behavior
of the offspring), hormone secretion (adrenocorticotropin hormone, corticosterone,
etc.), and protein and mRNA expression (for markers of neuronal activation and regulators
of the hypothalamic-pituitary-adrenal axis) within the brain. Once this mouse
maternal separation paradigm is established, we will take advantage of the powerful
genetic tools available in the mouse (including knockout and transgenic technologies)
to determine the interaction between environment, genetic, and epigenetic factors
governing brain development. This basic research has clinical biomedical relevance
as increasing evidence in humans suggests that early adverse experience contributes
to the vulnerability for a variety of psychopathologies particularly depression.
