Modulation of chloride homeostasis by inflammatory mediators in dorsal root ganglion neurons
Background:Chloride currents in peripheral nociceptive neurons have been implicated in the generation of afferent nociceptive signals, as Cl− accumulation in sensory endings establishes the driving force for depolarizing, and even excitatory, Cl− currents. The intracellular Cl− concentration can, ho...
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| Main Authors: | , , , , |
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| Format: | Article (Journal) |
| Language: | English |
| Published: |
12 August 2008
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| In: |
Molecular pain
Year: 2008, Volume: 4, Pages: 1-12 |
| ISSN: | 1744-8069 |
| DOI: | 10.1186/1744-8069-4-32 |
| Online Access: | Verlag, kostenfrei, Volltext: http://dx.doi.org/10.1186/1744-8069-4-32 Verlag, kostenfrei, Volltext: http://journals.sagepub.com/doi/10.1186/1744-8069-4-32 |
| Author Notes: | Katharina Funk, Anne Woitecki, Christina Franjic-Würtz, Thomas Gensch, Frank Möhrlen and Stephan Frings |
| Summary: | Background:Chloride currents in peripheral nociceptive neurons have been implicated in the generation of afferent nociceptive signals, as Cl− accumulation in sensory endings establishes the driving force for depolarizing, and even excitatory, Cl− currents. The intracellular Cl− concentration can, however, vary considerably between individual DRG neurons. This raises the question, whether the contribution of Cl− currents to signal generation differs between individual afferent neurons, and whether the specific Cl− levels in these neurons are subject to modulation. Based on the hypothesis that modulation of the peripheral Cl− homeostasis is involved in the generation of inflammatory hyperalgesia, we examined the effects of inflammatory mediators on intracellular Cl− concentrations and on the expression levels of Cl− transporters in rat DRG neurons.Results:We developed an in vitro assay for testing how inflammatory mediators influence Cl− concentration and the expression of Cl− transporters. Intact DRGs were... |
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| Item Description: | Gesehen am 15.05.2017 |
| Physical Description: | Online Resource |
| ISSN: | 1744-8069 |
| DOI: | 10.1186/1744-8069-4-32 |