The DOI matches its Crossref record; 58 of the 58 references it cites were found in a registry or an index.
Status Epilepticus Induces a Particular Microglial Activation State Characterized by Enhanced Purinergic Signaling
Open accessAbstract
Microglia cells are the resident macrophages of the CNS, and their activation plays a critical role in inflammatory reactions associated with many brain disorders, including ischemia, Alzheimer's and Parkinson's diseases, and epilepsy. However, the changes of microglia functional properties in epilepsy have rarely been studied. Here, we used a model of status epilepticus (SE) induced by intraperitoneal kainate injections to characterize the properties of microglial cells in hippocampal slices from CX3CR1 eGFP/+mice. SE induced within 3 h an increased expression of inflammatory mediators in the hippocampus, followed by a modification of microglia morphology, a microglia proliferation, and a significant neurodegeneration in CA1. Changes in electrophysiological intrinsic membrane properties of hippocampal microglia were detected at 24–48 h after SE with, in particular, the appearance of new voltage-activated potassium currents. Consistent with the observation of an upregulation of purinergic receptor mRNAs in the hippocampus, we also provide pharmacological evidence that microglia membrane currents mediated by the activation of P2 receptors, including P2X 7, P2Y 6, and P2Y 12, were increased 48 h after SE. As a functional consequence of this modification of purinergic signaling, motility of microglia processes toward a source of P2Y 12 receptor agonist was twice as fast in the epileptic hippocampus. This study is the first functional description of microglia activation in an in vivo model of inflammation and provides evidence for the existence of a particular microglial activation state after a status epilepticus.
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Cites
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BDNF from microglia causes the shift in neuronal anion gradient underlying neuropathic pain
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Cited by
Kettenmann, H., Hanisch, U.-K., Noda, M., & Verkhratsky, A. (2011) · Physiological Reviews · doi:10.1152/physrev.00011.2010 · Cited by 3,547
Microglia states and nomenclature: A field at its crossroads
Paolicelli, R. C., Sierra, A., Stevens, B., Tremblay, M.-E., Aguzzi, A., Ajami, B., Amit, I., Audinat, E., Bechmann, I., Bennett, M., et al. (2022) · Neuron · doi:10.1016/j.neuron.2022.10.020 · Cited by 1,973
Self-citationGlia and epilepsy: excitability and inflammation
Devinsky, O., Vezzani, A., Najjar, S., De Lanerolle, N. C., & Rogawski, M. A. (2013) · Trends in Neurosciences · doi:10.1016/j.tins.2012.11.008 · Cited by 867
Microglial Activation in Young Adults With Autism Spectrum Disorder
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Eyo, U. B., Peng, J., Swiatkowski, P., Mukherjee, A., Bispo, A., & Wu, L.-J. (2014) · Journal of Neuroscience · doi:10.1523/jneurosci.0416-14.2014 · Cited by 509
Metadata
- Authors
- Avignone, E., Ulmann, L., Levavasseur, F., Rassendren, F., & Audinat, E.
- Venue
- The Journal of Neuroscience
- Publisher
- Society for Neuroscience
- Published
- 2008-09-10
- Volume
- 28
- Issue
- 37
- Pages
- 9133-9144
- ISSN
- 0270-6474 (ISSN-L)
- 1529-2401
- OpenAlex
- W2110877402
- Cited by
- 287
- References
- 58
- FWCI
- 7.12
- Type
- journal article
- Language
- en
- Open access
- hybrid
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- Avignone, E., Ulmann, L., Levavasseur, F., Rassendren, F., & Audinat, E. (2008). Status Epilepticus Induces a Particular Microglial Activation State Characterized by Enhanced Purinergic Signaling. The Journal of Neuroscience. https://doi.org/10.1523/jneurosci.1820-08.2008
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