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Am J Physiol Heart Circ Physiol 275: H2053-H2063, 1998;
0363-6135/98 $5.00
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Vol. 275, Issue 6, H2053-H2063, December 1998

Stimulation of cerebellar fastigial nucleus inhibits interleukin-1beta -induced cerebrovascular inflammation

Elena Galea, Sara B. Glickstein, Douglas L. Feinstein, Eugene V. Golanov, and Donald J. Reis

Division of Neurobiology, Department of Neurology and Neuroscience, Cornell University Medical College, New York, New York 10021

Electrical stimulation of the cerebellar fastigial nucleus (FN) in rat protects the brain against ischemia. We studied whether FN could reduce the cerebrovascular inflammation as a mechanism of protection. FN or dentate nucleus (sham controls) was electrically stimulated for 1 h, and 72 h later rats were either injected with interleukin (IL)-1beta into the striata or processed to analyze inflammatory responses in isolated brain microvessels. In striata, IL-1beta induced a recruitment of leukocytes that was reduced by 50% by FN stimulation. In isolated microvessels, IL-1beta induced the transient and dose-dependent upregulation of the mRNAs encoding for the inducible nitric oxide synthase (NOS-2), intercellular adhesion molecule 1 (ICAM-1), and inhibitory kappa B-alpha (Ikappa B-alpha ), an inhibitor of nuclear factor-kappa B. FN stimulation decreased the upregulation of NOS-2 and ICAM-1 mRNAs, whereas it increased Ikappa B-alpha mRNA expression. Dentate nucleus stimulation did not mimic the FN actions. These findings suggest that FN stimulation may render brain microvessels refractory to IL-1beta by overproduction of Ikappa B-alpha and support the hypothesis that alteration of microvascular inflammation may contribute to the central neurogenic neuroprotection elicited from the FN.

blood-brain barrier; inducible nitric oxide synthase; inhibitory kappa B-alpha ; intercellular adhesion molecules; nuclear factor-kappa B


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