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Cerebellar stimulation reduces inducible nitric oxide synthase expression and protects brain from ischemia

Cerebellar stimulation reduces inducible nitric oxide synthase expression and protects brain from... Abstract A focal infarction produced by occlusion of the middle cerebral artery (MCAO) in spontaneously hypertensive rats induced expression of inducible nitric oxide synthase (iNOS) mRNA, measured by competitive reverse transcription-polymerase chain reaction. The mRNA appeared simultaneously in the ischemic core and penumbra at 8 h, peaked between 14 and 24 h, and disappeared by 48 h. At 24 h, inducible nitric oxide synthase (iNOS)-like immunoreactivity was present in the endothelium of cerebral microvessels and in scattered cells, probably representing leukocytes or activated microglia. Electrical stimulation of the cerebellar fastigial nucleus (FN) for 1 h, 48 h before MCAO, reduced infarct volumes by 45% by decreasing cellular death in the ischemic penumbra. It also reduced by >90% the expression of iNOS mRNA and protein in the penumbra, but not core, and decreased by 44% the iNOS enzyme activity. We conclude that excitation of neuronal networks represented in the cerebellum elicits a conditioned central neurogenic neuroprotection associated with the downregulation of iNOS mRNA and protein. This neuroimmune interaction may, by blocking the expression of iNOS, contribute to neuroprotection. cerebellum brain microvessels brain macrophages brain endothelium Footnotes Address for reprint requests: D. J. Reis, Div. of Neurobiology, Cornell University, 411 E 69th St., New York, NY 10021. All other correspondence to E. Galea, Anesthesiology Research Center (MC 519), Rm. 540, College of Medicine West Tower, 1819 W. Polk St., Chicago, IL 60612 (E-mail: egalea@uic.educ ). Copyright © 1998 the American Physiological Society http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png AJP - Heart and Circulatory Physiology The American Physiological Society

Cerebellar stimulation reduces inducible nitric oxide synthase expression and protects brain from ischemia

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Publisher
The American Physiological Society
Copyright
Copyright © 2011 the American Physiological Society
ISSN
0363-6135
eISSN
1522-1539
Publisher site
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Abstract

Abstract A focal infarction produced by occlusion of the middle cerebral artery (MCAO) in spontaneously hypertensive rats induced expression of inducible nitric oxide synthase (iNOS) mRNA, measured by competitive reverse transcription-polymerase chain reaction. The mRNA appeared simultaneously in the ischemic core and penumbra at 8 h, peaked between 14 and 24 h, and disappeared by 48 h. At 24 h, inducible nitric oxide synthase (iNOS)-like immunoreactivity was present in the endothelium of cerebral microvessels and in scattered cells, probably representing leukocytes or activated microglia. Electrical stimulation of the cerebellar fastigial nucleus (FN) for 1 h, 48 h before MCAO, reduced infarct volumes by 45% by decreasing cellular death in the ischemic penumbra. It also reduced by >90% the expression of iNOS mRNA and protein in the penumbra, but not core, and decreased by 44% the iNOS enzyme activity. We conclude that excitation of neuronal networks represented in the cerebellum elicits a conditioned central neurogenic neuroprotection associated with the downregulation of iNOS mRNA and protein. This neuroimmune interaction may, by blocking the expression of iNOS, contribute to neuroprotection. cerebellum brain microvessels brain macrophages brain endothelium Footnotes Address for reprint requests: D. J. Reis, Div. of Neurobiology, Cornell University, 411 E 69th St., New York, NY 10021. All other correspondence to E. Galea, Anesthesiology Research Center (MC 519), Rm. 540, College of Medicine West Tower, 1819 W. Polk St., Chicago, IL 60612 (E-mail: egalea@uic.educ ). Copyright © 1998 the American Physiological Society

Journal

AJP - Heart and Circulatory Physiology – The American Physiological Society

Published: Jun 1, 1998

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