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

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

Research output: Contribution to journalArticle

39 Scopus citations

Abstract

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)-1β into the striata or processed to analyze inflammatory responses in isolated brain microvessels. In striata, IL-1β induced a recruitment of leukocytes that was reduced by 50% by FN stimulation. In isolated microvessels, IL-1β 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 κB-α (IκB-α), an inhibitor of nuclear factor-κB, FN stimulation decreased the upregulation of NOS-2 and ICAM-1 mRNAs, whereas it increased IκB-α mRNA expression. Dentate nucleus stimulation did not mimic the FN actions. These findings suggest that FN stimulation may render brain microvessels refractory to IL-1β by overproduction of IκB-α and support the hypothesis that alteration of microvascular inflammation may contribute to the central neurogenic neuroprotection elicited from the FN.

Original languageEnglish (US)
Pages (from-to)H2053-H2063
JournalAmerican Journal of Physiology - Heart and Circulatory Physiology
Volume275
Issue number6 44-6
DOIs
StatePublished - Dec 1998

Keywords

  • Blood-brain barrier
  • Inducible nitric oxide synthase
  • Inhibitory κB- α
  • Intercellular adhesion molecules
  • Nuclear factor-κB

ASJC Scopus subject areas

  • Physiology
  • Physiology (medical)

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