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Vol. 303, Issue 3, 1061-1066, December 2002
Department of Pharmacology and Experimental Therapeutics (P.E.,
N.C., K.K., S.B., D.T., T.C.T), Department of Surgical Research (R.C.),
Department of Anatomy and Cell Biology (S.J.), and Department of
Internal Medicine (T.C.T.), Tufts University School of Medicine, New
England Medical Center, Boston, Massachusetts
Stress activates the hypothalamic-pituitary-adrenal axis through
release of corticotropin releasing hormone (CRH), leading to production
of glucocorticoids that down-regulate immune responses. Acute stress,
however, also has proinflammatory effects that seem to be mediated
through the activation of mast cells. Stress and mast cells have been
implicated in the pathophysiology of various inflammatory conditions,
including some in the central nervous system, such as multiple
sclerosis in which disruption of the blood-brain barrier (BBB) precedes
clinical symptoms. We previously showed that acute restraint stress
increases rat BBB permeability to intravenous 99Tc
gluceptate and that administration of the "mast cell stabilizer" disodium cromoglycate (cromolyn) inhibits this effect. In this study,
we show that the CRH-receptor antagonist Antalarmin blocks stress-induced 99Tc extravasation, whereas site-specific
injection of CRH in the paraventricular nucleus (PVN) of the
hypothalamus mimics acute stress. This latter effect is blocked by
pretreatment of the PVN with cromolyn; moreover, restraint stress
cannot disrupt the BBB in the diencephalon and cerebellum of
W/Wv mast cell-deficient mice. These results demonstrate
that CRH and mast cells are involved in regulating BBB permeability
and, possibly, brain inflammatory disorders exacerbated by acute stress.
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