Tarpley JW, Martin WJ, Baldwin BS, Forrest MJ, MacIntyre DE (2000) Contribution of IB4-positive sensory neurons to NGF-induced hyperalgesia in the rat. Neuroscience 2000 Abstracts 633.18. Society for Neuroscience, New Orleans, LA.
Summary: Sensory information is transmitted from the periphery to the spinal cord by distinct subsets of primary afferent neurons, including two major classes of C-fibers that are distinguished by their ability to bind the lectin IB4. IB4-positive neurons are primarily non-peptidergic, express the receptor tyrosine kinase, Ret, and are preferentially sensitive to the neurotrophic factor, GDNF. By contrast, the nerve growth factor (NGF) receptor tyrosine kinase, trkA, is predominantly expressed in IB4-negative neurons that contain substance P. Previous work suggested that depletion of IB4-positive neurons increases acute nociceptive thresholds to noxious thermal stimuli. The extent to which these non-peptidergic neurons mediate changes in nociception after injury is unknown. Here, we examined the contribution of IB4-positive, non-peptidergic, neurons to thermal and mechanical sensitivity after acute tissue injury. Baseline thermal (radiant heat) and mechanical (von Frey) thresholds were measured in rats prior to injection of IB4-saporin (5 ug/5 ul) into the left sciatic nerve. By two weeks, IB4-saporin-treated animals exhibited pronounced increases in their nociceptive thresholds to thermal and mechanical stimuli. At this time, treatment with NGF (5 ug/50 ul, i.pl.) increased paw thickness in both control and IB4-saporin-treated rats. However, nociceptive thresholds were significantly lowered in control rats, but not in those treated with IB4-saporin. This suggests that IB4-positive neurons contribute to injury-induced changes in thermal and mechanical sensitivity and provide insight into the function of this unique set of primary afferent neurons.
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