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The Journal of Neuroscience, September 24, 2003, 23(25):8706-8712

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Development/Plasticity/Repair
Chronic Neurotrophin-3 Strengthens Synaptic Connections to Motoneurons in the Neonatal Rat

Victor L. Arvanian,¹ Philip J. Horner,² Fred H. Gage,³ and Lorne M. Mendell¹

¹Department of Neurobiology and Behavior, State University of New York at Stony Brook, Stony Brook, New York 11794, ²Department of Neurological Surgery, University of Washington, Seattle, Washington 98104, and ³Laboratory of Genetics, The Salk Institute, La Jolla, California 92161

We report that neurotrophin-3 (NT-3), delivered chronically via fibroblasts implanted intrathecally into neonatal rats, can facilitate synaptic transmission in the spinal cord. A small collagen plug containing NT-3-secreting fibroblasts was placed on the exposed dorsal surface of the spinal cord (L1) of 2-d-old rats; controls received -galactosidase-secreting fibroblasts. After 6 hr to 12 d of survival, synaptic potentials (EPSP) elicited by two synaptic inputs, L5 dorsal root and ventrolateral funiculus (VLF), were recorded intracellularly in L5 motoneurons in vitro. Preparations treated with NT-3 implants exhibited enhanced monosynaptic synaptic transmission from both inputs, which persisted over the entire testing period. Unlike acute enhancement of transmission by NT-3 (Arvanian and Mendell, 2001a), the chronic effect could occur at connections not normally eliciting an NMDA receptor-mediated response at the time of NT-3 exposure. Using susceptibility to blockade of the NMDA receptor by Mg²⁺ and APV, we confirmed that chronic treatment with NT-3 did not enhance NMDA receptor activity at these connections. Cords treated with chronic NT-3 also transiently displayed polysynaptic components activated by VLF that were blocked by the NMDA receptor antagonist APV. These novel NMDA receptor-mediated potentials may reflect changes in interneurons near the site of fibroblast implantation. We conclude that chronic NT-3 enhances the potency of segmental and descending projections via mechanisms different from those underlying acute changes.

Key words: neurotrophin; NT-3; genetically engineered fibroblasts; synaptic transmission; plasticity; neonatal rat; development; motor neuron; spinal cord

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Received Dec 18, 2002; revised July 31, 2003; accepted August 5, 2003.

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