Vulchanova L, Stone LS, Olson T, Riedl MS, Elde R, Honda CN (1999) Depletion of IB4-binding sensory neurons results in elevated nociceptive thresholds. Neuroscience 1999 Abstracts 272.8. Society for Neuroscience, Miami, FL.
Summary: The lectin IB4 binds to and is specifically taken up by a subset of small sensory neurons, proposed to play a role in nociception. To examine the role of these neurons in sensory transmission we used a conjugate of IB4 and the toxin saporin (IB4-sap). IB4-sap (2 µg/5 µl) was injected in the left sciatic nerve of rats. Three days after the injection, the conjugate was visualized in the left L4 and L5 DRG using antisera to either the lectin or saporin. The cells labeled by these antisera were not stained by the Nissl-like marker ethidium bromide, suggesting disruption of their protein synthesis. Twenty one days after the injection there was a 36% reduction in the total number of neurons and a 50% reduction in IB4-binding neurons in L5 DRG of IB4-sap injected rats. Moreover, in dorsal horn of spinal cord, the projection site of the left sciatic nerve was devoid of IB4 binding. P2X3 immunostaining was also dramatically reduced, while the decrease in staining for SP, CGRP and VR1 was less pronounced. The responsiveness of the IB4-sap treated rats to noxious thermal and mechanical stimuli was examined using radiant heat and von Frey filaments, respectively. There was a significant increase in the withdrawal latency to thermal stimuli at day 10 and the withdrawal threshold to mechanical stimuli at day 14 post-treatment. By day 21 both the thermal and mechanical thresholds returned to baseline levels. We have shown that depletion of IB4-binding sensory neurons results in transient elevation of nociceptive thresholds. These findings suggest that IB4-binding neurons mediate the signaling of noxious stimuli and that an efficient compensatory mechanism appears to be activated within days of their loss. Supported by NIH grants DA09641 and DE07288.
Related Products: IB4-SAP (Cat. #IT-10)