主页 > 医学信息 >
【J Neurosci】癫痫持续可诱导一种以增强嘌呤能信
Correspondence should be addressed to Etienne Audinat, Laboratoire de Neurophysiologie et Nouvelles Microscopies, Inserm U603, Centre National de la Recherche Scientifique Unité Mixte de Recherche 8154, Université Paris Descartes, 45 rue des Saints-Pères, 75006 Paris, France. Email: etienne.audinat@univ-paris5.fr
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 CX3CR1eGFP/+ 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 P2X7, P2Y6, and P2Y12, were increased 48 h after SE. As a functional consequence of this modification of purinergic signaling, motility of microglia processes toward a source of P2Y12 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.
Key words: glial cells; ATP; inflammation; epilepsy; cytokines; hippocampus
--------------------------------------------------------------------------------
Received April 25, 2008; revised July 10, 2008; accepted Aug. 6, 2008.
http://www.jneurosci.org/cgi/content/abstract/28/37/9133 [标签:content1][标签:content2]
阅读本文的人还阅读：
作者:admin@医学,生命科学 2011-06-22 05:12
医学,生命科学网