Amb motiu del tancament d'estiu, la validació de documents es reprendrà a partir del 28 d'agost de 2026. Disculpeu les molèsties.
Con motivo del cierre de verano, la validación de documentos se reanudará a partir del 28 de agosto de 2026. Disculpad las molestias
Due to the summer closure, document validation will resume starting August 28, 2026. We apologize for any inconvenience.

Files

606754.pdf (629.86 KB)

Document type

Article

Version

Accepted version

Publication date

2012-02-24

All rights reserved

Please use this identifier to cite or link to this item: https://hdl.handle.net/2445/34278

ATP-dependent potassium channel blockade strengthens microglial neuroprotection after hypoxia-ischemia in rats.

Journal Title

Authors

Director/Tutor

Journal ISSN

Volume Title

Related resource

http://dx.doi.org/10.1016/j.expneurol.2012.02.010

Abstract

Stroke causes CNS injury associated with strong fast microglial activation as part of the inflammatory response. In rat models of stroke, sulphonylurea receptor blockade with glibenclamide reduced cerebral edema and infarct volume. We postulated that glibenclamide administered during the early stages of stroke might foster neuroprotective microglial activity through ATP-sensitive potassium (KATP) channel blockade. We found in vitro that BV2 cell line showed upregulated expression of KATP channel subunits in response to pro-inflammatory signals and that glibenclamide increases the reactive morphology of microglia, phagocytic capacity and TNFα release. Moreover, glibenclamide administered to rats 6, 12 and 24 h after transient Middle Cerebral Artery occlusion improved neurological outcome and preserved neurons in the lesioned core three days after reperfusion. Immunohistochemistry with specific markers to neuron, astroglia, microglia and lymphocytes showed that resident amoeboid microglia are the main cell population in that necrotic zone. These reactive microglial cells express SUR1, SUR2B and Kir6.2 proteins that assemble in functional KATP channels. These findings provide that evidence for the key role of KATP channels in the control of microglial reactivity are consistent with a microglial effect of glibenclamide into the ischemic brain and suggest a neuroprotective role of microglia in the early stages of stroke.

Subject

Micròglia, Canals de potassi, Isquèmia cerebral, Lesions cerebrals

Subject (English)

Microglia, Potassium channels, Cerebral ischemia, Brain damage

Citation

Collections

Articles publicats en revistes (Ciències Fisiològiques)

Citation

ORTEGA GONZÁLEZ, Fco. Javier, et al. ATP-dependent potassium channel blockade strengthens microglial neuroprotection after hypoxia-ischemia in rats. Experimental Neurology. 2012. Vol. 235, num. 1, pags. 282-296. ISSN 0014-4886. [consulted: 15 of August of 2026]. Available at: https://hdl.handle.net/2445/34278

Export metadata

JSON - METS

Share record