n-cofilin can compensate for the loss of adf in excitatory synapsesn-cofilin可以弥补损失的adf兴奋性突触.pdfVIP

N-Cofilin Can Compensate for the Loss of ADF in Excitatory Synapses ¨ 1. 1. 1. 2 Andreas Gorlich , Michael Wolf , Anika-Maria Zimmermann , Christine B. Gurniak , Mumna Al 3 ` 4 2 5 1 Banchaabouchi , Marco Sassoe-Pognetto , Walter Witke , Eckhard Friauf , Marco B. Rust * 1 Neurobiology/Neurophysiology Group, University of Kaiserslautern, Kaiserslautern, Germany, 2 Institute of Genetics, University of Bonn, Bonn, Germany, 3 Mouse Biology Unit, European Mouse Biology Laboratory, Monterotondo, Italy, 4 Department of Anatomy, Pharmacology and Forensic Medicine and National Institute of Neuroscience-Italy, University of Turin, Turin, Italy, 5 Animal Physiology Group, University of Kaiserslautern, Kaiserslautern, Germany Abstract Actin plays important roles in a number of synaptic processes, including synaptic vesicle organization and exocytosis, mobility of postsynaptic receptors, and synaptic plasticity. However, little is known about the mechanisms that control actin at synapses. Actin dynamics crucially depend on LIM kinase 1 (LIMK1) that controls the activity of the actin depolymerizing proteins of the ADF/cofilin family. While analyses of mouse mutants revealed the importance of LIMK1 for both pre- and postsynaptic mechanisms, the ADF/cofilin family member n-cofilin appears to be relevant merely for postsynaptic plasticity, and not for presynaptic physiology. By means of immunogold electron microscopy and immunocytochemistry, we here