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Rabies virus infection of cultured adult mouse dorsal root ganglion neurons
Castellanos, Jaime;Hurtado, Hernán;Arias, Janeth;Velandia, Alvaro;
Memórias do Instituto Oswaldo Cruz , 1996, DOI: 10.1590/S0074-02761996000500014
Abstract: an in vitro model of adult dorsal root ganglion neurons infection by rabies virus is described. viral marked neurotropism is observed, and the percentage and the degree of infection of the neurons is higher than in non neuronal cells, even if neurons are the minority of the cells in the culture. the neuritic tree is also heavily infected by the virus.
Prokineticin 2 potentiates acid-sensing ion channel activity in rat dorsal root ganglion neurons
Chun-Yu Qiu, Yu-QiangFang Liu, Fang Qiu, Jiliang Wu, Qun-Yong Zhou, Wang-Ping Hu
Journal of Neuroinflammation , 2012, DOI: 10.1186/1742-2094-9-108
Abstract: In the present study, experiments were performed on neurons freshly isolated from rat dorsal root ganglion by using whole-cell patch clamp and voltage-clamp recording techniques.PK2 dose-dependently enhanced proton-gated currents with an EC50 of 0.22?±?0.06 nM. PK2 shifted the proton concentration-response curve upwards, with a 1.81?±?0.11 fold increase of the maximal current response. PK2 enhancing effect on proton-gated currents was completely blocked by PK2 receptor antagonist. The potentiation was also abolished by intracellular dialysis of GF109203X, a protein kinase C inhibitor, or FSC-231, a protein interacting with C-kinase 1 inhibitor. Moreover, PK2 enhanced the acid-evoked membrane excitability of rat dorsal root ganglion neurons and caused a significant increase in the amplitude of the depolarization and the number of spikes induced by acid stimuli. Finally, PK2 exacerbated nociceptive responses to the injection of acetic acid in rats.These results suggest that PK2 increases the activity of acid-sensing ion channels via the PK2 receptor and protein kinase C-dependent signal pathways in rat primary sensory neurons. Our findings support that PK2 is a proalgesic factor and its signaling likely contributes to acidosis-evoked pain by sensitizing acid-sensing ion channels.
Cannabinoids Inhibit Acid-Sensing Ion Channel Currents in Rat Dorsal Root Ganglion Neurons  [PDF]
Yu-Qiang Liu, Fang Qiu, Chun-Yu Qiu, Qi Cai, Pengcheng Zou, Heming Wu, Wang-Ping Hu
PLOS ONE , 2012, DOI: 10.1371/journal.pone.0045531
Abstract: Local acidosis has been found in various pain-generating conditions such as inflammation and tissue injury. Cannabinoids exert a powerful inhibitory control over pain initiation via peripheral cognate receptors. However, the peripheral molecular targets responsible for the antinociceptive effects of cannabinoids are still poorly understood. Here, we have found that WIN55,212-2, a cannabinoid receptor agonist, inhibits the activity of native acid-sensing ion channels (ASICs) in rat dorsal root ganglion (DRG) neurons. WIN55,212-2 dose-dependently inhibited proton-gated currents mediated by ASICs. WIN55,212-2 shifted the proton concentration–response curve downwards, with an decrease of 48.6±3.7% in the maximum current response but with no significant change in the EC50 value. The inhibition of proton-gated current induced by WIN55,212-2 was almost completely blocked by the selective CB1 receptor antagonist AM 281, but not by the CB2 receptor antagonist AM630. Pretreatment of forskolin, an AC activator, and the addition of cAMP also reversed the inhibition of WIN55,212-2. Moreover, WIN55,212-2 altered acid-evoked excitability of rat DRG neurons and decreased the number of action potentials induced by acid stimuli. Finally, WIN55,212-2 attenuated nociceptive responses to injection of acetic acid in rats. These results suggest that WIN55,212-2 inhibits the activity of ASICs via CB1 receptor and cAMP dependent pathway in rat primary sensory neurons. Thus, cannabinoids can exert their analgesic action by interaction with ASICs in the primary afferent neurons, which was novel analgesic mechanism of cannabinoids.
Differing alterations of sodium currents in small dorsal root ganglion neurons after ganglion compression and peripheral nerve injury
Zhi-Jiang Huang, Xue-Jun Song
Molecular Pain , 2008, DOI: 10.1186/1744-8069-4-20
Abstract: Nerve injury produces dorsal root ganglion (DRG) neuron hyperexcitability, which is thought to underlie neuropathic pain by causing central sensitization. The voltage-gated sodium channels (VGSCs) can be dynamically regulated after axonal injury or peripheral inflammation and play important roles in modulating neural excitability [1,2]. The VGSCs are critically important for electrogenesis and nerve impulse conduction, and a target for important clinically relevant analgesics. However, mechanisms of the VGSCs contributing to hyperexcitability of DRG neurons and neuropathic pain remain unclear and the observations are controversial. For instance, inhibition or specific knock-down of tetrodotoxin-resistant (TTX-R) current Nav1.8 channel can effectively suppress neuropathic pain [3-5], while the Nav1.8 mRNA, protein and current are substantially decreased in DRG neurons in axotomized DRG neurons [6-9] or sciatic nerve injury [10]. The tetrodotoxin-sensitive (TTX-S) current Nav1.7 channel plays a critical role in various pain conditions [1], but nociceptors specific deletion of Nav1.7 did not eliminate neuropathic pain behavior in mice [11]. Thus, there is a need to further investigate roles of the VGSCs in different neuropathic pain conditions.Different from nerve injury models that produce injury to the peripheral axons of DRG neurons such as the chronic constriction injury (CCI) of the sciatic nerve, chronic compression of DRG (CCD) is used as an animal model that produces injury directly to DRG somata. We have shown that CCD treatment produces behavioral hyperalgesia and allodynia and DRG neuron hyperexcitability in rats [12-14]. However, ionic mechanisms contributing to CCD-induced neural hyperexcitability remain unclear. A recent study shows that TTX-R Na+ currents are upregulated in the cutaneous medium-sized CCD DRG neurons [15], which is somewhat different from the findings in axon injury models. The small DRG neurons most are nociceptive and play critical role
Different Concentration Selenium-modulated Action on Rat Dorsal Root Ganglion Neurons  [PDF]
Tong-Han Lan,Xian-Ming Liu
Pakistan Journal of Biological Sciences , 2005,
Abstract: In present study, a concentration-dependent effect of Selenium on rat dorsal root ganglion neurons was characterized using whole-cell patch-clamp recording. Among about 52% of the cells tested, the amplitude of membrane ion current increased, after administration of Selenium. In the presence of 0.001 nM (nanomolar) Selenium, the reversal potential and membrane conductance were changed. The above-mentioned actions suggest that selenium may play a physiological role in regulating the excitatory action on mammalian neurons.
Pharmacological evaluation of rat dorsal root ganglion neurons as an in vitro model for diabetic neuropathy  [cached]
Eve Peeraer,An Van Lutsenborg,An Verheyen,et al
Journal of Pain Research , 2011,
Abstract: Eve Peeraer1,2, An Van Lutsenborg3, An Verheyen1,4, Raf De Jongh5, Rony Nuydens1, Theo F Meert1,21Johnson & Johnson Pharmaceutical Research and Development, Beerse, Belgium; 2University Hasselt, Hasselt, Belgium; 3Free University Brussels, Brussels, Belgium; 4The Vesalius Research Center, University of Leuven, Leuven, Belgium; 5Intensive Care and Emergency Care, Ziekenhuis Oost-Limburg, Genk, BelgiumBackground: Diabetic neuropathy is a complication of diabetes mellitus that develops in about 50% of people with diabetes. Despite its widespread occurrence and devastating effects, this complication is still not fully understood, and there is no treatment available to prevent its development.Methods: In this study, immunocytochemistry for activating transcription factor 3, a marker for cell injury, was used to investigate the stress response in dorsal root ganglion neurons in both in vitro and ex vivo models of diabetic neuropathy.Results: Our findings showed increased activating transcription factor 3 expression in hyperglycemic culture conditions and in dorsal root ganglion neurons isolated from diabetic rats. Glial cell line-derived neurotrophic factor, a substance with known neuroprotective properties, was able to reduce diabetes mellitus-induced neuronal stress in vitro, while gabapentin and carbamazepine, currently used to treat neuropathic pain, showed only limited effects.Conclusion: Growth factors may have a therapeutic benefit as neurotrophic agents in the treatment of diabetic peripheral neuropathy, but gabapentin and carbamazepine have no direct protective effect on sensory neurons. This research also indicates that immunocytochemistry for activating transcription factor 3 is a valuable tool for evaluation of pharmacological substances in dorsal root ganglion cultures.Keywords: diabetic peripheral neuropathy, dorsal root ganglion, activating transcription factor 3, glial cell line-derived neurotrophic factor, anticonvulsants
Pharmacological evaluation of rat dorsal root ganglion neurons as an in vitro model for diabetic neuropathy
Eve Peeraer, An Van Lutsenborg, An Verheyen, et al
Journal of Pain Research , 2011, DOI: http://dx.doi.org/10.2147/JPR.S15452
Abstract: rmacological evaluation of rat dorsal root ganglion neurons as an in vitro model for diabetic neuropathy Original Research (4532) Total Article Views Authors: Eve Peeraer, An Van Lutsenborg, An Verheyen, et al Published Date February 2011 Volume 2011:4 Pages 55 - 65 DOI: http://dx.doi.org/10.2147/JPR.S15452 Eve Peeraer1,2, An Van Lutsenborg3, An Verheyen1,4, Raf De Jongh5, Rony Nuydens1, Theo F Meert1,2 1Johnson & Johnson Pharmaceutical Research and Development, Beerse, Belgium; 2University Hasselt, Hasselt, Belgium; 3Free University Brussels, Brussels, Belgium; 4The Vesalius Research Center, University of Leuven, Leuven, Belgium; 5Intensive Care and Emergency Care, Ziekenhuis Oost-Limburg, Genk, Belgium Background: Diabetic neuropathy is a complication of diabetes mellitus that develops in about 50% of people with diabetes. Despite its widespread occurrence and devastating effects, this complication is still not fully understood, and there is no treatment available to prevent its development. Methods: In this study, immunocytochemistry for activating transcription factor 3, a marker for cell injury, was used to investigate the stress response in dorsal root ganglion neurons in both in vitro and ex vivo models of diabetic neuropathy. Results: Our findings showed increased activating transcription factor 3 expression in hyperglycemic culture conditions and in dorsal root ganglion neurons isolated from diabetic rats. Glial cell line-derived neurotrophic factor, a substance with known neuroprotective properties, was able to reduce diabetes mellitus-induced neuronal stress in vitro, while gabapentin and carbamazepine, currently used to treat neuropathic pain, showed only limited effects. Conclusion: Growth factors may have a therapeutic benefit as neurotrophic agents in the treatment of diabetic peripheral neuropathy, but gabapentin and carbamazepine have no direct protective effect on sensory neurons. This research also indicates that immunocytochemistry for activating transcription factor 3 is a valuable tool for evaluation of pharmacological substances in dorsal root ganglion cultures.
Effects of Mechanical Force on Cytoskeleton Structure and Calpain-Induced Apoptosis in Rat Dorsal Root Ganglion Neurons In Vitro  [PDF]
Zhengxu Ye, Yuqing Wang, Xin Quan, Jing Li, Xueyu Hu, Jinghui Huang, Zhuojing Luo
PLOS ONE , 2012, DOI: 10.1371/journal.pone.0052183
Abstract: Background A sudden mechanical insult to the spinal cord is usually caused by changing pressure on the surface of the spinal cord. Most of these insults are mechanical force injuries, and their mechanism of injury to the spinal cord is largely unknown. Methods Using a compression-driven instrument to simulate mechanical force, we applied mechanical pressure of 0.5 MPa to rat dorsal root ganglion (DRG) neurons for 10 min to investigate cytoskeletal alterations and calpain-induced apoptosis after the mechanical force injury. Results The results indicated that mechanical forces affect the structure of the cytoskeleton and cell viability, induce early apoptosis, and affect the cell cycle of DRG neurons. In addition, the calpain inhibitor PD150606 reduced cytoskeletal degradation and the rate of apoptosis after mechanical force injury. Conclusion Thus, calpain may play an important role in DRG neurons in the regulation of apoptosis and cytoskeletal alterations induced by mechanical force. Moreover, cytoskeletal alterations may be substantially involved in the mechanotransduction process in DRG neurons after mechanical injury and may be induced by activated calpain. To our knowledge, this is the first report to demonstrate a relationship between cytoskeletal degradation and apoptosis in DRG neurons.
Modulation of chloride homeostasis by inflammatory mediators in dorsal root ganglion neurons
Katharina Funk, Anne Woitecki, Christina Franjic-Würtz, Thomas Gensch, Frank M?hrlen, Stephan Frings
Molecular Pain , 2008, DOI: 10.1186/1744-8069-4-32
Abstract: We developed an in vitro assay for testing how inflammatory mediators influence Cl- concentration and the expression of Cl- transporters. Intact DRGs were treated with 100 ng/ml NGF, 1.8 μM ATP, 0.9 μM bradykinin, and 1.4 μM PGE2 for 1–3 hours. Two-photon fluorescence lifetime imaging with the Cl--sensitive dye MQAE revealed an increase of the intracellular Cl- concentration within 2 hours of treatment. This effect coincided with enhanced phosphorylation of the Na+-K+-2Cl- cotransporter NKCC1, suggesting that an increased activity of that transporter caused the early rise of intracellular Cl- levels. Immunohistochemistry of NKCC1 and KCC2, the main neuronal Cl- importer and exporter, respectively, exposed an inverse regulation by the inflammatory mediators. While the NKCC1 immunosignal increased, that of KCC2 declined after 3 hours of treatment. In contrast, the mRNA levels of the two transporters did not change markedly during this time. These data demonstrate a fundamental transition in Cl- homeostasis toward a state of augmented Cl- accumulation, which is induced by a 1–3 hour treatment with inflammatory mediators.Our findings indicate that inflammatory mediators impact on Cl- homeostasis in DRG neurons. Inflammatory mediators raise intracellular Cl- levels and, hence, the driving force for depolarizing Cl- efflux. These findings corroborate current concepts for the role of Cl- regulation in the generation of inflammatory hyperalgesia and allodynia. As the intracellular Cl- concentration rises in DRG neurons, afferent signals can be boosted by excitatory Cl- currents in the presynaptic terminals. Moreover, excitatory Cl- currents in peripheral sensory endings may also contribute to the generation or modulation of afferent signals, especially in inflamed tissue.The regulation of intracellular chloride, [Cl-]i, in DRG neurons has a distinct impact on the detection and transmission of the peripheral nociceptive signals. Measurements with isolated DRG neurons have sh
Axotomy-Induced miR-21 Promotes Axon Growth in Adult Dorsal Root Ganglion Neurons  [PDF]
Iain T. Strickland, Louise Richards, Fiona E. Holmes, David Wynick, James B. Uney, Liang-Fong Wong
PLOS ONE , 2011, DOI: 10.1371/journal.pone.0023423
Abstract: Following injury, dorsal root ganglion (DRG) neurons undergo transcriptional changes so as to adopt phenotypic changes that promote cell survival and axonal regeneration. Here we used a microarray approach to profile changes in a population of small noncoding RNAs known as microRNAs (miRNAs) in the L4 and L5 DRG following sciatic nerve transection. Results showed that 20 miRNA transcripts displayed a significant change in expression levels, with 8 miRNAs transcripts being altered by more than 1.5-fold. Using quantitative reverse transcription PCR, we demonstrated that one of these miRNAs, miR-21, was upregulated by 7-fold in the DRG at 7 days post-axotomy. In dissociated adult rat DRG neurons lentiviral vector-mediated overexpression of miR-21 promoted neurite outgrowth on a reduced laminin substrate. miR-21 directly downregulated expression of Sprouty2 protein, as confirmed by Western blot analysis and 3′ untranslated region (UTR) luciferase assays. Our data show that miR-21 is an axotomy-induced miRNA that enhances axon growth, and suggest that miRNAs are important players in regulating growth pathways following peripheral nerve injury.
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