This Article Full Text (PDF) References Alert me when this article is cited Alert me if a correction is posted Services Email this article to a friend Similar articles in this journal Similar articles in Web of Science Similar articles in PubMed Alert me to new issues of the journal Add to Saved Citations Download to citation manager Request Permissions Request Reprints Add to My Marked Citations Citing Articles Citing Articles via Google Scholar Citing Articles via Scopus Google Scholar Articles by Monnet-Tschudi, F. Articles by Honegger, P. Search for Related Content PubMed PubMed Citation Articles by Monnet-Tschudi, F. Articles by Honegger, P. Social Bookmarking                         What's this?

Neurotoxicant-induced inflammatory response in three-dimensional brain cell cultures

Department of Physiology, University of Lausanne, Lausanne, Switzerland, Florianne.Tschudi-Monnet{at}unil.ch

M-G. Zurich

Department of Physiology, University of Lausanne, Lausanne, Switzerland

P. Honegger

Department of Physiology, University of Lausanne, Lausanne, Switzerland

Brain inflammatory response is triggered by the activation of microglial cells and astrocytes in response to various types of CNS injury, including neurotoxic insults. Its outcome is determined by cellular interactions, inflammatory mediators, as well as trophic and/or cytotoxic signals, and depends on many additional factors such as the intensity and duration of the insult, the extent of both the primary neuronal damage and glial reactivity and the developmental stage of the brain. Depending on particular circumstances, the brain inflammatory response can promote neuroprotection, regeneration or neurodegeneration. Glial reactivity, regarded as the central phenomenon of brain inflammation, has also been used as an early marker of neurotoxicity. To study the mechanisms underlying the glial reactivity, serum-free aggregating brain cell cultures were used as an in vitro model to test the effects of conventional neurotoxicants such as organophosphate pesticides, heavy metals, excitotoxins and mycotoxins. This approach was found to be relevant and justified by the complex cell—cell interactions involved in the brain inflammatory response, the variability of the glial reactions and the multitude of mediators involved. All these variables need to be considered for the elucidation of the specific cellular and molecular reactions and their consequences caused by a given chemical insult. Human & Experimental Toxicology (2007) 26, 339—346

Key Words: aggregating brain cell cultures • astrocyte • brain inflammation • chlorpyrifos • fumonisin B1 (FB1) • glial fibrillary acidic protein (GFAP) • glial reactivity • gliosis • lead • mercury • microglia • mycotoxins • ochratoxin A (OTA) • organophosphate pesticides (OPs) • parathion • trimethyltin (TMT)

Human & Experimental Toxicology, Vol. 26, No. 4, 339-346 (2007)
DOI: 10.1177/0960327107074589


CiteULike    Complore    Connotea    Del.icio.us    Digg    Reddit    Technorati    Twitter    What's this?