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- W2496754534 endingPage "488" @default.
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- W2496754534 abstract "This chapter reviews that modulation of neuronal Clˉ homeostasis serves as a mechanistic link between central neuroimmune response and neuronal excitability: via the release of BDNF acting on neuronal TrkB, microglia cause a depolarizing shift in reversal potential for GABA A and glycine receptor-mediated currents effectively impairing, and, in some cases, even inverting, inhibition. This results in an imbalance of inputs towards excitation, raising neuronal network excitability. Thus, by regulating Clˉ homeostasis in their neighboring neurons, microglial cells can effectively control neuronal network excitability. The findings outlined in this chapter also highlight the fact that Clˉ homeostasis does not only change during development, or as a consequence of direct injury to neurons, but that it can be regulated by signaling mechanisms in adult tissue. This microglia-to-neuron communication pathway was unveiled at the level of the spinal cord in an experimental model of chronic pain. To describe the cascade of neuron-to-microglia-to-neuron signaling mechanisms that eventually lead to altered Clˉ homeostasis, it focuses mainly on spinal mechanism underlying neuropathic pain, but these findings are likely to be relevant to other syndromes that involve neuroimmune interactions in other CNS areas including epilepsy, multiple sclerosis, spinal cord injury and brain ischemia." @default.
- W2496754534 created "2016-08-23" @default.
- W2496754534 creator A5017328884 @default.
- W2496754534 date "2010-01-01" @default.
- W2496754534 modified "2023-09-25" @default.
- W2496754534 title "Modulation of Chloride Homeostasis by Microglia" @default.
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- W2496754534 doi "https://doi.org/10.1016/b978-0-12-374373-2.00023-6" @default.
- W2496754534 hasPublicationYear "2010" @default.
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