Glial cell line-derived neurotrophic factor contributes to delayed inflammatory hyperalgesia in adjuvant rat pain model

Fang, Ming; Wang, Y.; He, Qihua; Sun, Yiyuan; Deng, Li; Wang, X.M.; Han, Ji-Sheng

doi:10.1016/s0306-4522(02)00958-2

Cited by 50 publications

(32 citation statements)

References 54 publications

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“…However, it should be noted that a 15 d intrathecal application of high concentrations (12 g/d) of GDNF caused a reduction in neuropathic pain after peripheral nerve injury (Boucher et al, 2000). Conversely, injection of an antibody to GDNF decreased hyperalgesia after complete Freund's adjuvant injection (Fang et al, 2003). Clearly, the route of administration and experimental model are critical factors in the evaluation of GDNF action in the sensory system.…”

Section: Discussionmentioning

confidence: 99%

Glial Cell Line-Derived Neurotrophic Factor Expression in Skin Alters the Mechanical Sensitivity of Cutaneous Nociceptors

Albers¹,

Woodbury²,

Ritter³

et al. 2006

J. Neurosci.

104

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Neurons classified as nociceptors are dependent on nerve growth factor (NGF) during embryonic development, but a large subpopulation lose this dependence during embryonic and postnatal times and become responsive to the transforming growth factor ␤ family member, glial cell line-derived growth factor (GDNF). To elucidate the functional properties of GDNF-dependent nociceptors and distinguish them from nociceptors that retain NGF dependence, the cellular and physiologic properties of sensory neurons of wild-type and transgenic mice that overexpress GDNF in the skin (GDNF-OE) were analyzed using a skin, nerve, dorsal root ganglion, and spinal cord preparation, immunolabeling, and reverse transcriptase-PCR assays. Although an increase in peripheral conduction velocity of C-fibers in GDNF-OE mice was measured, other electrophysiological properties, including resting membrane potential and somal action potentials, were unchanged. We also show that isolectin B4 (IB4)-positive neurons, many of which are responsive to GDNF, exhibited significantly lower thresholds to mechanical stimulation relative to wild-type neurons. However, no change was observed in heat thresholds for the same population of cells. The increase in mechanical sensitivity was found to correlate with significant increases in acid-sensing ion channels 2A and 2B and transient receptor potential channel A1, which are thought to contribute to detection of mechanical stimuli. These data indicate that enhanced expression of GDNF in the skin can change mechanical sensitivity of IB4-positive nociceptive afferents and that this may occur through enhanced expression of specific types of channel proteins.

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Section: Discussionmentioning

confidence: 99%

Glial Cell Line-Derived Neurotrophic Factor Expression in Skin Alters the Mechanical Sensitivity of Cutaneous Nociceptors

Albers¹,

Woodbury²,

Ritter³

et al. 2006

J. Neurosci.

104

View full text Add to dashboard Cite

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“…To ensure that this effect at 24 hours on the contralateral paw was not due to the trauma of IA injection, tests were performed on mice in which 10 l saline had been injected IA into one knee joint and the other joint left untreated. At 24 hours, neither hind paw exhibited a change in thermal hyperalgesic threshold (data not shown), thus suggesting that the observed change seen in the contralateral paw at 24 hours may have been due to bilateral hyperalgesia (23)(24)(25). Throughout the time course, the TRPV1 Ϫ/Ϫ mice exhibited no change in thermal hyperalgesic thresholds from baseline levels, whereas it was not until 2 weeks that the threshold returned to normal in the paws of the CFA-treated WT mice ( Figure 5).…”

Section: Trpv1 In Joint Inflammationmentioning

confidence: 96%

Involvement of transient receptor potential vanilloid 1 in the vascular and hyperalgesic components of joint inflammation

Keeble¹,

Russell²,

Curtis³

et al. 2005

Arthritis & Rheumatism

154

117

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Objective. To investigate the endogenous involvement of transient receptor potential vanilloid 1 (TRPV1) in a model of knee joint inflammation in the mouse.Methods. Following characterization of wild-type (WT) and TRPV1-knockout mice, inflammation was induced via intraarticular (IA) injection of Freund's complete adjuvant (CFA). Knee swelling was assessed as diameter, and inflammatory heat hyperalgesia was determined using the Hargreaves technique, for up to 3 weeks. At 18 hours, acute hyperpermeability was measured with 125 I-albumin, and cytokines and myeloperoxidase activity, a marker of neutrophils, were assayed in synovial fluid extracts. The possibility that exogenous tumor necrosis factor ␣ (TNF␣) was involved in influencing TRPV1 activation was investigated in separate experiments.Results. Increased levels of knee swelling, hyperpermeability, leukocyte accumulation, and TNF␣ were found in WT mice 18 hours after IA CFA treatment compared with saline treatment. Significantly less knee swelling and hyperpermeability were found in TRPV1 ؊/؊ mice, but leukocyte accumulation and TNF␣ levels were similar in WT and TRPV1 ؊/؊ mice. Knee swelling in response to CFA remained significantly higher for a longer period in WT mice compared with TRPV1 ؊/؊ mice, with thermal hyperalgesic sensitivity observed at 24 hours and at 1 week in WT, but not TRPV1 ؊/؊ , mice. Knee swelling was attenuated (P < 0.05) in TRPV1 ؊/؊ compared with WT mice 4 hours after IA administration of TNF␣.Conclusion. Our findings indicate that TRPV1 has a role in acute and chronic inflammation in the mouse knee joint. Thus, selective antagonism of TRPV1 should be considered as a potential target for treatment of acute and chronic joint inflammation.

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“…Thus, neurotrophic factors can enhance axonal growth in different models of SCI, and each one may play a distinct role in modulating neural function with certain redundancy. Nonetheless, eventual clinical application of neurotrophic factors may encounter limitations because of side effects such as hyperalgesia associated with NGF [95].…”

Section: Strategy 4: Application Of Neurotrophic Factors and Viral Vementioning

confidence: 99%

Strategies to Create a Regenerating Environment for the Injured Spinal Cord

Xiang¹,

Pan²,

Kastin³

2005

CPD

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Spine cord injury (SCI) leads to devastating functional loss below the level of injury. Partially explained by the presence of a non-permissive environment, the injured spinal cord does not mount adequate regeneration to re-establish functional connections. Therefore, it is important to identify the cellular and molecular factors and their interactions that affect axonal regeneration within the changed environment. This review will discuss the current understanding of the neuronal and glial factors and the extracellular matrix in the spinal cord that inhibit axonal growth, and it will summarize some major approaches for facilitation of regeneration. The strategies are classified into the following categories: penetration of the blood-brain barrier; modulation of caspase activity to reduce apoptosis; stem cells and tissue implantation; administration of neurotrophic factors, including viral vector-mediated delivery; and modulation of the extracellular matrix. Although recent studies on genomic regulation and apoptosis have identified particularly important molecular targets, more is necessary to achieve long-term regeneration. A combination of the approaches targeting various aspects in the regenerating environment would be more effective than a single strategy. Overall, insights arising from the experimental results may eventually lead to better therapeutic intervention so as to lessen the functional disability and enhance the quality of life in patients with SCI.

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Glial cell line-derived neurotrophic factor contributes to delayed inflammatory hyperalgesia in adjuvant rat pain model

Cited by 50 publications

References 54 publications

Glial Cell Line-Derived Neurotrophic Factor Expression in Skin Alters the Mechanical Sensitivity of Cutaneous Nociceptors

Glial Cell Line-Derived Neurotrophic Factor Expression in Skin Alters the Mechanical Sensitivity of Cutaneous Nociceptors

Involvement of transient receptor potential vanilloid 1 in the vascular and hyperalgesic components of joint inflammation

Strategies to Create a Regenerating Environment for the Injured Spinal Cord

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