Differentially expressed genes in rat dorsal root ganglia following peripheral nerve injury

Kim, Dong–Sun; Lee, Sang-Ji; Park, So-Yun; Yoo, Hea-Jin; Kim, Shin-Hee; Kim, Kwang‐Jin; Cho, Hee-Jung

doi:10.1097/00001756-200110290-00050

Cited by 40 publications

(20 citation statements)

References 27 publications

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“…These classes of molecules have also been identified by others using similar experimental approaches [46,47]. Specific signal transduction pathways are involved in almost every cellular process [48].…”

Section: Discussionmentioning

confidence: 84%

Identification of regeneration-associated genes after central and peripheral nerve injury in the adult rat

et al. 2003

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Section: Discussionmentioning

confidence: 84%

Identification of regeneration-associated genes after central and peripheral nerve injury in the adult rat

et al. 2003

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“…Bennett originally reported [92] that this model likely involved the presence of spontaneous pain, since appetite was suppressed and spontaneous nocifensive behaviors frequently occurred, but such nonevoked behaviors are neither common nor easily measured. This model has been used for a great number (>300) and variety of studies since its first description, to examine both the development of spinal and supraspinal sensitization following CCI [102][103][104][105] and its genetic basis [106][107][108][109], as well as to examine a number of potential therapeutic interventions [19,110,111] for the partial nerve-injury-related pain.…”

Section: Peripheral Nerve Injury Testsmentioning

confidence: 99%

Common animal models for spasticity and pain

Eaton¹

2003

JRRD

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Abstract-Animal models of spasticity and pain have allowed for the elucidation of possible mechanisms and the evaluation of potential therapeutic interventions for these serious clinical problems. Each model mirrors the clinical appearance of many features of the syndrome, but few reproduce the myriad patient reports of either intensity or relevant contributing factors, especially in models of chronic neuropathic pain. Often these models have been used to predict the potency and efficacy of pharmacologic agents that work in human pain states. Pain models have relied on measurements of the shifts in behavioral hypersensitivity to tactile and thermal stimuli, tests that are not used quantitatively in human patients. Even with the multiple peripheral and central models of spasticity and pain used in animals, only a few actually test human conditions: namely, diabetic neuropathy, chemotherapy, and immunotherapy for tumors. However, all these models have allowed for the comparison of certain behavioral, cellular, biochemical, and molecular mechanisms with human patient populations. Here we review the few extant models of spasticity, nerve injury, and central injury models of pain, and describe their features and use.

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“…Alterations in nerve function, responsiveness, activity, neurotransmitter and receptor expression, morphology, and synaptic connections contribute to the allodynia, hyperalgesia, and spontaneous pain that characterize neuropathic pain states (Woolf and Salter, 2000; Zimmermann, 2001; Campbell and Meyer, 2006; Scholz and Woolf, 2007). Long-lasting modifications in pain transmission pathways develop as a result of global changes in gene expression in specific neuronal and glial cells (Newton et al, 2000; Kim et al, 2001; Costigan et al, 2002; Wang et al, 2002; Xiao et al, 2002). However, it is largely unknown how nerve injury brings about such global changes in gene expression to induce chronic pain.…”

Section: Introductionmentioning

confidence: 99%

Changes in expression of sensory organ-specific microRNAs in rat dorsal root ganglia in association with mechanical hypersensitivity induced by spinal nerve ligation

et al. 2009

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Chronic neuropathic pain caused by peripheral nerve injury is associated with global changes in gene expression in damaged neurons. To understand the molecular mechanisms underlying neuropathic pain, it is essential to elucidate how nerve injury alters gene expression and how the change contributes to the development and maintenance of chronic pain. MicroRNAs are non-protein-coding RNA molecules that regulate gene expression in a wide variety of biological processes mainly at the level of translation. This study investigated the possible involvement of microRNAs in gene regulation relevant to neuropathic pain. The analyses focused on a sensory organ-specific cluster of microRNAs that includes miR-96, -182, and -183. RT-PCR analyses confirmed that these microRNAs were highly enriched in the dorsal root ganglion (DRG) of adult rats. Using the L5 spinal nerve ligation (SNL) model of chronic neuropathic pain, we observed a significant reduction in expression of these microRNAs in injured DRG neurons compared to controls. In situ hybridization and immunohistochemical analyses revealed that these microRNAs are expressed in both myelinated (N52 positive) and unmyelinated (IB4 positive) primary afferent neurons. They also revealed that the intracellular distributions of the microRNAs in DRG neurons were dramatically altered in animals with mechanical hypersensitivity. Whereas microRNAs were uniformly distributed within the DRG soma of non-allodynic animals, they were preferentially localized to the periphery of neurons in allodynic animals. The redistribution of microRNAs was associated with changes in the distribution of the stress granule protein TIA-1. These data demonstrate that SNL induces changes in expression levels and patterns of miR-96, -182, and -183, implying their possible contribution to chronic neuropathic pain through translational regulation of pain-relevant genes. Moreover, stress granules were suggested to be assembled and associated with microRNAs after SNL, which may play a role in modification of microRNA-mediated gene regulation in DRG neurons.

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Differentially expressed genes in rat dorsal root ganglia following peripheral nerve injury

Cited by 40 publications

References 27 publications

Identification of regeneration-associated genes after central and peripheral nerve injury in the adult rat

Identification of regeneration-associated genes after central and peripheral nerve injury in the adult rat

Common animal models for spasticity and pain

Changes in expression of sensory organ-specific microRNAs in rat dorsal root ganglia in association with mechanical hypersensitivity induced by spinal nerve ligation

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