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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 · kg 1 · 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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