Patch clamp reveals powerful blockade of the mitochondrial permeability transition pore by the D2-receptor agonist pramipexole Iqbal Sayeed 1 , Suhel Parvez 1 , Kirstin Winkler-Stuck, Gordon Seitz, Isabelle Trieu, Claus-Werner Wallesch, Peter Schönfeld * and Detlef Siemen 2 Departments of Neurology and * Biochemistry, University of Magdeburg, D-39120 Magdeburg, Germany 2 Correspondence: Department of Neurology, University of Magdeburg, Leipziger Str. 44, D-39120 Magdeburg, Germany. E-mail: detlef.siemen@medizin.uni-magdeburg.de <h3>SPECIFIC AIMS</h3> The motor scores in Parkinson’s disease decline slower if the patients are treated with dopamine agonists instead of L -dopa. We wanted to see if this protective effect could be explained by the inhibition of the cascade leading to apoptotic cell death with the mitochondrial permeability transition pore (PTP) as a potential target. <h3>PRINCIPAL FINDINGS</h3> <h3>1. Proving the identity of the PTP by dose-dependent cyclosporin A (CSA) blockade</h3> It could be inhibition of the PTP that causes the neuroprotective effect of the dopamine-D2 agonist pramipexole (PPX). We prepared mitoplasts (swollen and deenergized mitochondria devoid of their outer membrane by hypotonic treatment) from rat liver mitochondria (RLM) and applied patch-clamp techniques in the mitoplast-attached mode for measuring single-channel currents. Almost every second patch with sufficient seal resistance showed a distinct
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Patch clamp reveals powerful blockade of the mitochondrial permeability transition pore by the D2-receptor agonist pramipexole
Sayeed, Iqbal; Parvez, Suhel; Winkler-Stuck, Kirstin; Seitz, Gordon; Trieu, Isabelle; Wallesch, Claus-Werner; Schönfeld, Peter; Siemen, Detlef
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, Volume 20 (3): 556
Fed of American Socs for Experimental Biology – Mar 1, 2006
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