Peripheral inflammation and neuroprotection: Systemic pretreatment with complete Freund's adjuvant reduces 6-hydroxydopamine toxicity in a rodent model of Parkinson's disease

M. T. Armentero, Giovanna Levandis, Giuseppe Nappi, Eleonora Bazzini, Fabio Blandini

Research output: Contribution to journalArticle

Abstract

Complete Freund's adjuvant (CFA), a pro-inflammatory agent, was inoculated, subcutaneously, to Sprague-Dawley rats prior to the intrastriatal injection of 6-hydroxydopamine (6-OHDA). Animals were sacrificed 7 and 28 days following 6-OHDA injection; neuronal damage, glial activation and cytokine levels, within the nigrostriatal system, were then investigated. Nigrostriatal degeneration induced by 6-OHDA was accompanied by early microglial and astroglial activation, which preceded the onset of dopaminergic cell loss, in the SNc, without significant changes in cytokine levels. CFA pretreatment markedly reduced the SNc neuronal loss and associated microglial activation, as well as the rotational response to apomorphine. These changes were associated with moderate, transient increases in the nigrostriatal levels of glial-cell-derived neurotrophic factor (GDNF) and pro-inflammatory cytokines, including interleukin (IL)-1α, IL-1β and IL-6. Our results show that prior delivery of a peripheral, pro-inflammatory stimulus induces neuroprotection, in a rodent model of Parkinson's disease, possibly through the modulation of cytokine production at the nigrostriatal level.

Original languageEnglish
Pages (from-to)492-505
Number of pages14
JournalNeurobiology of Disease
Volume24
Issue number3
DOIs
Publication statusPublished - Dec 2006

Keywords

  • Astroglia
  • Cytokines
  • GDNF
  • Microglia
  • Neurodegeneration
  • Striatum
  • Substantia nigra pars compacta
  • Tyrosine hydroxylase

ASJC Scopus subject areas

  • Neurology

Fingerprint Dive into the research topics of 'Peripheral inflammation and neuroprotection: Systemic pretreatment with complete Freund's adjuvant reduces 6-hydroxydopamine toxicity in a rodent model of Parkinson's disease'. Together they form a unique fingerprint.

  • Cite this