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Role of IB4-binding sensory neurons in the effects of intradermal capsaicin injection.
Vulchanova L, Olson TH, Elde R, Honda CN (2000) Role of IB4-binding sensory neurons in the effects of intradermal capsaicin injection. Neuroscience 2000 Abstracts 212.7. Society for Neuroscience, New Orleans, LA.
Summary: We have shown previously that a unilateral injection of a conjugate of the lectin IB4 and the toxin saporin (IB4-SAP) into sciatic nerve of rats results in loss of IB4-binding neurons and transient increase in thermal and mechanical nociceptive thresholds. The thresholds were maximally increased 10 days post-treatment and returned to baseline levels by day 21. In the present study, we examined the responses of IB4-SAP treated rats after intradermal injection of capsaicin, which results in acute nocifensive behavior followed by thermal and mechanical hyperalgesia. The nocifensive behavior of IB4-SAP treated rats 10, 21 and 42 days post-treatment was 6%, 36% and 47%, respectively, of the behavior of control treated rats. IB4-SAP treated rats injected with capsaicin did not develop thermal or mechanical hyperalgesia at any of the time points examined. These results suggest that the increase in thermal nociceptive thresholds after IB4-SAP treatment is due to loss of VR1-expressing IB4-binding neurons since the nocifensive behavior is most likely mediated by the capsaicin receptor VR1, which also transduces noxious thermal stimuli. In addition, VR1 in surviving neurons may contribute to the recovery of thermal nociceptive thresholds. Finally, our results suggest that IB4-binding neurons are required for development of capsaicin-mediated hyperalgesia, and that the recovery of the responsiveness of IB4-SAP treated rats to noxious stimuli under normal conditions is not accompanied by recovery of the mechanisms underlying hyperalgesia.
Related Products: IB4-SAP (Cat. #IT-10)
Depletion of IB4-binding sensory neurons results in elevated nociceptive thresholds.
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)
Distinct neurochemical features of acute and persistent pain.
Basbaum AI (1999) Distinct neurochemical features of acute and persistent pain. Proc Natl Acad Sci U S A 96:7739-7743. doi: 10.1073/pnas.96.14.7739
Related Products: IB4-SAP (Cat. #IT-10)
Tackling pain at the source: New ideas about nociceptors.
Snider WD, McMahon SB (1998) Tackling pain at the source: New ideas about nociceptors. Neuron 20:629-632. doi: 10.1016/s0896-6273(00)81003-x
Related Products: IB4-SAP (Cat. #IT-10)