Page 121 - Biobehavioral Resilence to Stress

98 Biobehavioral Resilience to Stress

including hypertension, cardiovascular disease, and disorders of immune
function.
Conversely, it appears that individuals who are resilient to stress are able
to maintain SNS activation within a more conservative window of eff ective
but adaptive responsiveness. It has been proposed that such individuals are
activated to an extent that is strong enough to respond effectively to danger

but moderate enough to avoid incapacitation, depression, anxiety, and debil-
itating fear (Charney, 2004; Morgan III et al., 2002; Southwick, Vythilingam
& Charney, 2005). Dienstbier (1991), summarizing data from multiple stud-
ies, has proposed that performance is enhanced during optimal SNS activa-
tion: relatively low levels of baseline epinephrine with robust increases in
epinephrine and norepinephrine (NE) in response to challenges, followed by
relatively rapid return to baseline levels.
Neuropeptide Y (NPY), an amino acid that is released with NE when the
SNS is strongly activated, is one of the neurochemicals that helps to main-
tain SNS activity within an optimal activation range (reviewed by Southwick

et al., 1999). One effect of NPY is to inhibit the continued release of NE so
that the SNS does not overshoot. Preliminary studies of highly resilient
special operations soldiers (special forces) have shown that during extremely
stressful training scenarios, high levels of NPY are associated with better
performance (Morgan III et al., 2000, 2002). It is possible that rapid and
marked increases in NE among these soldiers are held in check by robust
increases in NPY.
By contrast, researchers have observed reduced levels of NPY among
combat veterans diagnosed with PTSD (Rasmusson et al., 2000). When the
SNS is stressed or provoked, these individuals demonstrate an associated
increase in NE, but the accompanying release of NPY may be inadequate
to hold the rising levels of NE in check. Numerous neurobiological stud-
ies strongly suggest that an increase in NE can contribute to an exagger-
ated increase in heart rate, blood pressure, respiratory rate, anxiety, panic,
vigilance, and intrusive trauma-related memories (reviewed in Southwick et

al., 1999). Thus, it appears that NPY plays a role in mediating resilience to
stress.
Galanin, a peptide that is involved in neuroendocrine control, cardio-
vascular regulation, food intake, pain control, learning and memory, and
anxiety may also be associated with resilience to stress. Like NPY, galanin is
coexpressed in a high percentage of noradrenergic neurons and tends to be
released when NE activity is high. In rats, central administration of galanin
reduces the firing rate of the locus coeruleus, which contains more than half

of the brain’s noradrenergic neurons, and when injected into the amygdala

blocks the anxiogenic effects of stress (Bing, Moller, Engel, Soderpalm &

Heilig, 1993; MÖller, Sommer, Thorsell & Heilig, 1999). The overall net eff ect
of NE hyperactivity may thus depend on the balance between NE, NPY, and

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