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Volume 17, Number 1, Issue of January 1, 1997 pp. 372-382
Copyright ©1997 Society for Neuroscience

Neurotrophin-3 Administration Attenuates Deficits of Pyridoxine-Induced Large-Fiber Sensory Neuropathy

Received June 27, 1996; revised Oct. 18, 1996; accepted Oct. 22, 1996.

Maureen E. Helgren, Kenneth D. Cliffer, Kim Torrento, Chris Cavnor, Rory Curtis, Peter S. DiStefano, Stanley J. Wiegand, and Ronald M. Lindsay

Regeneron Pharmaceuticals, Inc., Tarrytown, New York 10591-6707

Chronic treatment of adult rats for 2-3 weeks with high doses of pyridoxine (vitamin B₆) produced a profound proprioceptive loss, similar to that found in humans overdosed with this vitamin or treated with the chemotherapeutic agent cisplatin. Pyridoxine toxicity was manifest as deficits in simple and precise locomotion and sensory nerve function and as degeneration of large-diameter/large-fiber spinal sensory neurons. As assessed quantitatively in a beam-walking task and by EMG recording of H waves evoked by peripheral nerve stimulation, coadministration of the neurotrophic factor neurotrophin-3 (NT-3; 5-20 mg · kg¹ · d¹, s.c.) during chronic pyridoxine treatment largely attenuated the behavioral and electrophysiological sequelae associated with pyridoxine toxicity. Furthermore, NT-3 administration prevented degeneration of sensory fibers in the dorsal column of the spinal cord. These data are consistent with the evidence that NT-3 is a target-derived neurotrophic factor for muscle sensory afferents and suggest that pharmacological doses of NT-3 may be beneficial in the treatment of large-fiber sensory neuropathies.

Key words: NT-3; sensory neuropathy; proprioception; DRG; pyridoxine; sensory-motor function

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