Differential Changes in TRPV1 Expression After Trigeminal Sensory Nerve Injury

Kim, Hyun Yeong; Park, Chul-Kyu; Cho, Ik‐Hyun; Jung, Sung Jun; Kim, Joong Soo; Oh, Seog Bae

doi:10.1016/j.jpain.2007.11.013

Cited by 74 publications

(54 citation statements)

References 32 publications

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“…Recent research has indicated that TRPV1 in the TG plays an important role in different types of pain [21][22]. Furthermore, previous research has considered pain receptors in the parodontium to primarily be the free nerve endings of primary sensory neurons.…”

Section: Discussionmentioning

confidence: 99%

Blocking of TRPV-1 in the parodontium relieves orthodontic pain by inhibiting the expression of TRPV-1 in the trigeminal ganglion during experimental tooth movement in rats

Gao

Liu

Zhang

et al. 2016

Neuroscience Letters

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Section: Discussionmentioning

confidence: 99%

Blocking of TRPV-1 in the parodontium relieves orthodontic pain by inhibiting the expression of TRPV-1 in the trigeminal ganglion during experimental tooth movement in rats

Gao

Liu

Zhang

et al. 2016

Neuroscience Letters

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“…Injury is thought to activate intrinsic neuronal growth programs, including neurotrophin signaling, to promote axon regrowth (59). Neurotrophin release in response to injury also leads to inflammatory signaling, hyperalgesia, and aberrant sprouting in peripheral sensory neurons, resulting in potentially debilitating neuropathic pain (60)(61)(62)(63)(64)(65)(66)(67). Increased expression of TRPV2 was thought to contribute directly to pain sensation after nerve injury (58).…”

Section: Discussionmentioning

confidence: 99%

Nerve Growth Factor Regulates Transient Receptor Potential Vanilloid 2 via Extracellular Signal-Regulated Kinase Signaling To Enhance Neurite Outgrowth in Developing Neurons

Cohen

Johnson

Pilat

et al. 2015

Molecular and Cellular Biology

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Neurite outgrowth is key to the formation of functional circuits during neuronal development. Neurotrophins, including nerve growth factor (NGF), increase neurite outgrowth in part by altering the function and expression of Ca 2؉ -permeable cation channels. Here we report that transient receptor potential vanilloid 2 (TRPV2) is an intracellular Ca 2؉ -permeable TRPV channel upregulated by NGF via the mitogen-activated protein kinase (MAPK) signaling pathway to augment neurite outgrowth. TRPV2 colocalized with Rab7, a late endosome protein, in addition to TrkA and activated extracellular signal-regulated kinase (ERK) in neurites, indicating that the channel is closely associated with signaling endosomes. In line with these results, we showed that TRPV2 acts as an ERK substrate and identified the motifs necessary for phosphorylation of TRPV2 by ERK. Furthermore, neurite length, TRPV2 expression, and TRPV2-mediated Ca 2؉ signals were reduced by mutagenesis of these key ERK phosphorylation sites. Based on these findings, we identified a previously uncharacterized mechanism by which ERK controls TRPV2-mediated Ca 2؉ signals in developing neurons and further establish TRPV2 as a critical intracellular ion channel in neuronal function.E stablishment of precise neural connections during nervous system development is essential in forming functional circuits. Neurite outgrowth allows for connection and communication between developing neurons and their targets. In the developing peripheral nervous system, nerve growth factor (NGF) is a targetderived extracellular cue necessary for outgrowth (1). Upon binding to its extracellular receptor, NGF activates the phosphoinositide 3-kinase (PI3K) signaling pathway, which is essential for the survival of developing neurons, and the mitogen-activated protein kinase (MAPK) pathway, which promotes differentiation and neurite outgrowth (2, 3). These signaling pathways have numerous downstream effectors in developing neurons, including several Ca 2ϩ -permeable transient receptor potential (TRP) channels (4-8).Thermosensitive TRP channels from the vanilloid subfamily (thermoTRPV channels) consist of four nonselective Ca 2ϩ -permeable cation channels, TRP vanilloid 1 (TRPV1) to TRPV4, originally described as pain and temperature sensors in adult sensory neurons (9-12). Recent evidence suggests, however, that only TRPV1 functions as a molecular sensor of heat and painful stimuli in vivo, while the function of TRPV2 to -4 remains unclear (13-16). TRPV2 and TRPV4 have also been detected in developing peripheral neurons, suggesting that they may play a role in growth programs during development (17, 18). Consistent with this notion, TRPV2 has been implicated in axon outgrowth (18), and critical mutations in TRPV4 result in peripheral axonal neuropathies (19,20). Despite these initial findings, the details by which thermoTRPV channels influence neuronal development remain unknown.Here we explore the molecular mechanisms by which thermoTRPV channels contribute to neurotrophin-mediated peripher...

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“…The increase in TRPV1- and CGRP-LI in the DRGs occurs with a parallel increase in the spinal cord dorsal horn. Interestingly, increased immunoreactivity for TRPV1 [62, 79, 80] and CGRP [56, 81] has been previously shown in uninjured primary afferent neuronal perikarya in different models of nerve lesion. Moreover, CGRP expression may increase in several pathological conditions, including partial nerve injury, where pain hypersensitivity occurs [82–86].…”

Section: Discussionmentioning

confidence: 99%

Bortezomib Treatment Produces Nocifensive Behavior and Changes in the Expression of TRPV1, CGRP, and Substance P in the Rat DRG, Spinal Cord, and Sciatic Nerve

Quartu

Carozzi

Dorsey

et al. 2014

BioMed Research International

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To investigate neurochemical changes associated with bortezomib-induced painful peripheral neuropathy (PN), we examined the effects of a single-dose intravenous administration of bortezomib and a well-established “chronic” schedule in a rat model of bortezomib-induced PN. The TRPV1 channel and sensory neuropeptides CGRP and substance P (SP) were studied in L4-L5 dorsal root ganglia (DRGs), spinal cord, and sciatic nerve. Behavioral measures, performed at the end of the chronic bortezomib treatment, confirmed a reduction of mechanical nociceptive threshold, whereas no difference occurred in thermal withdrawal latency. Western blot analysis showed a relative increase of TRPV1 in DRG and spinal cord after both acute and chronic bortezomib administration. Reverse transcriptase-polymerase chain reaction revealed a decrease of TRPV1 and CGRP mRNA relative levels after chronic treatment. Immunohistochemistry showed that in the DRGs, TRPV1-, CGRP-, and SP-immunoreactive neurons were mostly small- and medium-sized and the proportion of TRPV1- and CGRP-labeled neurons increased after treatment. A bortezomib-induced increase in density of TRPV1- and CGRP-immunoreactive innervation in the dorsal horn was also observed. Our findings show that bortezomib-treatment selectively affects subsets of DRG neurons likely involved in the processing of nociceptive stimuli and that neurochemical changes may contribute to development and persistence of pain in bortezomib-induced PN.

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Differential Changes in TRPV1 Expression After Trigeminal Sensory Nerve Injury

Cited by 74 publications

References 32 publications

Blocking of TRPV-1 in the parodontium relieves orthodontic pain by inhibiting the expression of TRPV-1 in the trigeminal ganglion during experimental tooth movement in rats

Blocking of TRPV-1 in the parodontium relieves orthodontic pain by inhibiting the expression of TRPV-1 in the trigeminal ganglion during experimental tooth movement in rats

Nerve Growth Factor Regulates Transient Receptor Potential Vanilloid 2 via Extracellular Signal-Regulated Kinase Signaling To Enhance Neurite Outgrowth in Developing Neurons

Bortezomib Treatment Produces Nocifensive Behavior and Changes in the Expression of TRPV1, CGRP, and Substance P in the Rat DRG, Spinal Cord, and Sciatic Nerve

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