Page 119 - Biobehavioral Resilence to Stress

96 Biobehavioral Resilience to Stress

The hypothalamus is a nexus for inputs from the rest of the brain, and

serves as a regulatory center for many physical processes and systems, includ-
ing responses to emotional stimuli and stress. The amygdala plays a critical

role in mediating fear and aggression. The amygdala also sends signals that
activate autonomic and hormonal responses to stress. These signals are asso-

ciated with behavioral responses to stress, including “freezing” in response
to danger (LeDoux, 1996). Cells in the amygdala undergo physical changes
(remodeling of dendrites and synaptic connections) in response to repeated
stress. In addition, there is recent evidence to indicate that a single exposure
to traumatic stress may provoke new synapse formation or retraction in the
amygdala and that such changes are accompanied by aggressive and anxious
behavior (McEwen & Chattarji, 2004). For example, exposure to a single acute
immobilization stress for the first time in a rat’s life causes increased anxi-

ety that can be measured 10 days later, along with increased density of spine
synapses in the amygdala (Vyas, Mitra, Shankaranarayana Rao & Chattarji,

2002). Similar effects have been observed to last for weeks in rats aft er expo-
sure to a natural predator such as a cat (Adamec, Burton, Shallow & Budgell,
1998; Mesches, Fleshner, Heman, Rose & Diamond, 1999), and there is evi-

dence for lasting effects of such exposure on autonomic, neuroendocrine,
and behavioral indices (Korte, Koolhaas, Wingfield & McEwen, 2005).

The hippocampus is a brain structure that is essential to memory. Th e
hippocampus works together with the amygdala to store information about
“where we were and what we were doing” at the time of an emotionally

charged event. The hippocampus also plays a key role in spatial naviga-
tion and memories of events in daily life. When exposed to chronic stress,
the hippocampus itself undergoes structural remodeling; hippocampal
cells demonstrate changes in spine synapse density, dendrite branch-
ing, and length (McEwen, 1999). These changes are accompanied by defi -

cits in hippocampal-dependent memory (Conrad, LeDoux, Magariños &
McEwen, 1999).
The prefrontal cortex acts as a master control region for both autonomic

and neuroendocrine responses to stress. Prefrontal cortical processes also
serve to limit impulsive behavior and support executive functions such as

decision-making and the shifting of attention to newly relevant stimuli
that predict reward or punishment (Damasio, 1997). Repeated stress causes
remodeling of prefrontal neuronal dendrites and synaptic connections;
these changes are accompanied by impairment in tests of mental fl exibility

and attention shifting (Liston et al., 2006; Radley et al., 2005; Wellman,

2001). Although the predominant effect of repeated stress is retraction of
dendrites and spines, there is also evidence for stress-induced expansion of
dendrites in the orbitofrontal cortex. Dendrites and spines in the prefron-
tal cortex may respond rapidly to acute stressors (Izquierdo, Wellman &
Holmes, 2006).

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