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Vol. 294, Issue 1, 103-116, July 2000
Psychiatric Institute, Department of Psychiatry, College of
Medicine, University of Illinois at Chicago, Chicago, Illinois
Alterations in hypothalamic-pituitary-adrenal (HPA) function are
associated with changes in mood and behavior. Protein kinase A (PKA),
on activation, phosphorylates many important intracellular proteins and
thereby plays a major role in mediating various physiological functions
in brain. We systematically examined the relationship of altered HPA
function with PKA modifications in rat brain after administering
corticosterone to normal rats and by first adrenalectomizing rats and
then simultaneously treating them with different doses of
corticosterone. Rats were decapitated on day 1, 4, or 14. Subcutaneously implanted 50- or 100-mg corticosterone pellets in normal
rats for 4 or 14 days significantly decreased PKA activity,
Bmax of [3H]cyclic AMP
binding, and protein levels of selective PKA regulatory (RI
, RII
)
and catalytic (Cat) subunit isoforms in cortex and hippocampus in a
dose-dependent manner without any significant changes at day 1; these
changes were more pronounced at day 14. However, adrenalectomy caused
the opposite changes in these measures at day 4 or 14 in both cortex
and hippocampus, and the magnitude of the changes was more pronounced
at day 14. Simultaneous treatment with implanted corticosterone at 50- or 100-mg doses in adrenalectomized rats reversed the
adrenalectomy-induced increases in PKA measures in a dose-dependent
manner. These results suggest that endogenous glucocorticoid modifies
the expression of RI, RII, and Cat subunit isoforms of PKA, as
well as the catalytic and regulatory activities of PKA, and that these
alterations in PKA may in part explain HPA axis-mediated changes in
mood and behavior.
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