| STRESS HISTORY AND PUBERTAL DEVELOPMENT INTERACT TO
SHAPE HYPOTHALAMIC--PITUITARY--ADRENAL AXIS PLASTICITY |
| R.D.Romeo1*; R.Bellani1,2;
I.N.Karatsoreos3; N.Chhua1; M.Vernov1;
C.D.Conrad2; B.S.McEwen1 |
| 1. Lab Neuroendocrinol., Rockefeller Univ, New York, NY,
USA |
| 2. Dept Psych, Arizona State Univ., Tempe, AZ, USA |
| 3. Dept Psych, Columbia Univ., New York, NY, USA |
|
Stress reactivity changes dramatically during puberty.
For instance, levels of adrenocorticotropic hormone (ACTH) and corticosterone
(CORT) following a single, acute exposure to stress take 45-60 min
longer to return to baseline in prepubertal animals compared to adults.
In addition to development, experience with stressors can also influence
stress reactivity. To assess possible interactions between pubertal
development and experience on stress reactivity, we compared hormonal
and central stress responsiveness in prepubertal (28 days of age)
and adult (77 days of age) male rats exposed to either acute (30 min)
or chronic (30 min/day for 7d) restraint stress. In support of previous
studies, we found prepubertal males had significantly longer ACTH
and CORT (total and free) responses compared to adults in reaction
to a single 30 min session of restraint. Interestingly, however, in
reaction to chronic stress, prepubertal animals had peak ACTH and
CORT (total and free) responses that were 2.5 times greater, but more
quickly terminated, when compared to adults. Using Fos immunohistochemistry
we assessed neuronal activation in key brain regions involved in regulating
HPA function. Accompanying the profound difference in stress reactivity
at these two ages, stress-induced Fos expression in the paraventricular
nucleus of the hypothalamus (PVN) was significantly higher in prepubertal
males compared to adults after acute or chronic restraint. As the
PVN is composed of a number of distinct functional cell groups, we
are currently investigating the phenotype of these differentially
activated cells in the prepubertal and adult PVN. Taken together,
these data indicate that pubertal maturation and stress history interact
to shape stress responsiveness, and provide a model to study relatively
rapid and robust neuroendocrine plasticity.
Support Contributed By: MH 065749, MH58911, MH41256, and MH 064727
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