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Neurology 2001;57:324-327
© 2001 American Academy of Neurology


Brief Communications

Labeling of rat neurons by anti-GluR3 IgG from patients with Rasmussen encephalitis

C. Frassoni, PhD;, R. Spreafico, MD, PhD;, S. Franceschetti, MD;, N. Aurisano, PhD, P. Bernasconi, PhD;, R. Garbelli, PhD;, C. Antozzi, MD;, S. Taverna, PhD;, T. Granata, MD and R. Mantegazza, MD

From the Department of Experimental Neurophysiology and Epileptology (Drs. Frassoni, Spreafico, Franceschetti, Garbelli, and Taverna), Myopathology and Immunology Unit (Drs. Aurisano, Bernasconi, and Mantegazza), Department of Neuromuscular Diseases (Dr. Antozzi), and Department of Child Neurology (Dr. Granata), Istituto Nazionale Neurologico "Carlo Besta," Milan, Italy.

Address correspondence and reprint requests to Dr. R. Spreafico, Department of Experimental Neurophysiology and Epileptology, Istituto Nazionale Neurologico "Carlo Besta," Via Celoria 11, 20133 Milan, Italy; e-mail: spreafico{at}istituto-besta.it

The authors report the immunocytochemical localization in rat brain of affinity-purified anti-GluR3 (glutamate receptor) antibodies from two patients with Rasmussen encephalitis (RE) and from immunized rabbits. The distribution of immunolabeling was similar using antibodies from rabbits and patients with RE. No electrophysiologic responses were elicited from acutely dissociated kainate-responsive neurons isolated from rat brain when these antibodies were applied. These findings show that anti-GluR3 antibodies purified from patients with RE bind to specific regions of the CNS but do not act through an excitotoxic mechanism.




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