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Featured Article: Biotinylated targeting: A viable option?
Lappi DA (2003) Featured Article: Biotinylated targeting: A viable option?. Targeting Trends 4(2)
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Loss of IB4 staining in dorsal root ganglion neurons after spinal nerve ligation is not the result of cell death.
Arunkumar R, Ackerman LL, Jones III R, Holdsworth R, Proudfit HK, Hammond DL (2002) Loss of IB4 staining in dorsal root ganglion neurons after spinal nerve ligation is not the result of cell death. IASP 2002 Abstracts International Association for the Study of Pain, San Diego, CA.
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Loss of IB4-positive sensory neurons mitigates the consequences of nerve injury in the rat.
Tarpley JW, MacIntyre E, Martin WJ (2002) Loss of IB4-positive sensory neurons mitigates the consequences of nerve injury in the rat. IASP 2002 Abstracts International Association for the Study of Pain, San Diego, CA.
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Cytotoxic targeting of isolectin IB4-binding sensory neurons.
Vulchanova L, Olson TH, Stone LS, Riedl MS, Elde R, Honda CN (2001) Cytotoxic targeting of isolectin IB4-binding sensory neurons. Neuroscience 108(1):143-155. doi: 10.1016/s0306-4522(01)00377-3 PMID: 11738138
Summary: Vulchanova et al. examine the role of IB4-binding neurons in nociception. IB4-SAP (Cat. #IT-10) was injected into rats (2 µg in left sciatic nerve). The resulting ablation of IB4-binding neurons provides evidence for their role in nociceptive processing and demonstrates a rapid compensatory response to signalling of acute pain.
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Capsaicin-sensitive inhibitory pathway in rat spinal cord dorsal horn.
Gu JG, Nakatsuka T, Tanaka E, Takeda D, Jennifer LX (2001) Capsaicin-sensitive inhibitory pathway in rat spinal cord dorsal horn. Neuroscience 2001 Abstracts 158.13. Society for Neuroscience, San Diego, CA.
Summary: The inhibitory system in the spinal cord plays an important role in regulating nociceptive sensory inputs. Here we examined inhibitory synaptic activity in lamina V neurons of the spinal dorsal horn following the activation of capsaicin VR1 receptors. Experiments were performed with spinal cord slice preparations and inhibitory postsynaptic currents (IPSCs) were recorded using patch-clamp technique. Bath application of capsaicin (2 μM) increased the amplitude and frequency of GABAergic and glycinergic spontaneous IPSCs in the majority of lamina V neurons tested. The effects of capsaicin were completely antagonized by capsazepine (10 μM), and were also blocked in the presence of tetrodotoxin (0.5 μM). However, when CNQX (20 μM) and APV (100 μM) were used to block glutamatergic synaptic transmission, the effects of capsaicin were not abolished. Furthermore, after the injection of IB4-saporin into sciatic nerve to remove IB4-positive C-primary afferent terminals, capsaicin still increased sIPSC frequency in the presence of CNQX and APV. These results suggest that inhibitory pathway could be recruited in the absence of glutamatergic inputs from primary afferents. The release of neuropeptides from capsaicin-sensitive C-primary afferents may activate GABAergic and glycinergic interneurons in superficial laminae, and the inhibitory activity may be further forwarded to lamina V neurons. The capsaicin-sensitive inhibitory pathway may play an important role in the control of nociceptive transmission in the spinal cord.
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α,β-methylene ATP sensitive P2X receptor mediated enhancement of glutamate release from the central terminals of Aδ primary afferents onto lamina V neurons in rat spinal cord.
Nakatsuka T, Takeda D, Gu JG (2001) α,β-methylene ATP sensitive P2X receptor mediated enhancement of glutamate release from the central terminals of Aδ primary afferents onto lamina V neurons in rat spinal cord. Neuroscience 2001 Abstracts 158.16. Society for Neuroscience, San Diego, CA.
Summary: We examined the role of αβmATP-sensitive P2X receptors in modulating glutamate release from sensory synapses of the spinal cord by using whole-cell patch-clamp recordings from dorsal horn neurons in lamina V region. The majority of lamina V neurons synapsed with terminals expressing αβmATP-sensitive P2X receptors. Application of P2X receptor agonist 100 μM αβmATP resulted in a large increase in mEPSC frequency. The increases in mEPSC frequency by αβmATP were completely abolished by the P2X receptor antagonist 10 μM PPADS, but were not blocked by Ca2+ channel blocker 30 μM La3+. αβmATP remained to be effective in increasing mEPSC frequency after the removal of superficial dorsal horn (lamina I-III) or after the injection of IB4-saporin into sciatic nerve to remove P2X3 expressing afferent terminals. Furthermore, we found that αβmATP-sensitive synapses of lamina V neurons were associated with central terminals derived from Aδ primary afferents. The EPSCs evoked by dorsal root stimulation at Aδ-fiber intensity were potentiated by 1 μM αβmATP as well as by the ecto-ATPase inhibitor 10 μM ARL67156, and depressed in the presence of 10 μM PPADS and 5 μM suramin. These results suggest that αβmATP-sensitive P2X receptors play a significant role in modulating excitatory synaptic transmission in the spinal cord.
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Contribution of IB4-positive sensory neurons to NGF-induced hyperalgesia in the rat.
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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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.
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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.
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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
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