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PubMed 20383592


Referenced in Channelpedia wiki pages of: none

Automatically associated channels: Kv10.1 , Slo1



Title: Reduced PBR/TSPO expression after minocycline treatment in a rat model of focal cerebral ischemia: a PET study using [(18)F]DPA-714.

Authors: Abraham Martín, Raphael Boisgard, Michael Kassiou, Frédéric Dollé, Bertrand Tavitian

Journal, date & volume: Mol Imaging Biol, 2011 Feb , 13, 10-5

PubMed link: http://www.ncbi.nlm.nih.gov/pubmed/20383592


Abstract
Many new candidate pharmaceuticals designed to improve recovery after stroke have been proposed recently, but there are still too few molecular imaging methods capable to assess their efficacy. A hallmark of the inflammatory reaction that follows focal cerebral ischemia is overexpression of the mitochondrial peripheral benzodiazepine receptor/18 kDa translocator protein (PBR/TSPO) in the monocytic lineage and astrocytes. This overexpression can be imaged with positron emission tomography (PET) using PBR/TSPO-selective radioligands such as [(18)F]DPA-714.Here, we tested whether PET with [(18)F]DPA-714 would evidence the effect of minocycline, a broad spectrum antibiotic presently tested as neuroprotective agent after stroke, on the inflammatory reaction induced in an experimental model of stroke.Ten rats were subjected to a 2-h transient middle cerebral artery occlusion with reperfusion. Minocycline or saline was intravenously administrated 1 h after reperfusion and daily during the following 6 days. PET studies were performed using [(18)F]DPA-714 at 7 days after cerebral ischemia.In vivo PET imaging showed a significant decrease in [(18)F]DPA-714 uptake at 7 days after cerebral ischemia in rats treated with minocycline with respect to saline-treated animals. Minocycline treatment had no effect on the size of the infarcted area.Minocycline administered daily during 7 days after ischemia decreases [(18)F]DPA-714 binding, suggesting that the drug exerts an anti-inflammatory activity. [(18)F]DPA-714 PET is a useful biomarker to study novel anti-inflammatory strategies in experimental cerebral ischemia.