Connexin 36 promotes cortical spreading depolarization and ischemic brain damage

Panagiotis Bargiotas; Sajjad Muhammad; Mahbubur Rahman; Nurith Jakob; Raimund Trabold; Elke Fuchs; Lothar Schilling; Nikolaus Plesnila; Hannah Monyer; Markus Schwaninger

doi:10.1016/j.brainres.2012.08.046

Connexin 36 promotes cortical spreading depolarization and ischemic brain damage

Panagiotis Bargiotas, Sajjad Muhammad, Mahbubur Rahman, Nurith Jakob, Raimund Trabold, Elke Fuchs, Lothar Schilling, Nikolaus Plesnila, Hannah Monyer, Markus Schwaninger^*

^*Corresponding author for this work

Institute of Experimental and Clinical Pharmacology and Toxicology

12 Citations (Scopus)

Abstract

Cortical spreading depolarization (CSD) promotes the progression of neuronal injury after cerebral ischemia. However, the mechanisms of propagation of postischemic CSD events are still unclear. In this study we characterized the role of the main neuronal gap junction protein connexin 36 (Cx36) in generating postischemic CSDs. In Cx36-deficient mice and controls we occluded the distal middle cerebral artery. To detect CSD events we recorded the direct current and laser Doppler flow. In addition, locomotor function and the infarct size were determined. Cx36-deficient mice had significantly fewer and shorter CSD events than wild-type controls. Additionally, Cx36 deletion is neuroprotective, leading to a better functional outcome and decreased infarct size after ischemia. These results suggest a detrimental role for Cx36 after ischemia, possibly by promoting CSD.

Original language	English
Journal	Brain Research
Volume	1479
Pages (from-to)	80-85
Number of pages	6
ISSN	0006-8993
DOIs	https://doi.org/10.1016/j.brainres.2012.08.046
Publication status	Published - 15.10.2012

Funding

The research leading to these results received funding from the European Union's Seventh Framework Program (FP7/2007–2013) under Grant agreements 201024 and 202213 (European Stroke Network).

UN SDGs

This output contributes to the following UN Sustainable Development Goals (SDGs)

SDG 3 Good Health and Well-being

Research Areas and Centers

Academic Focus: Center for Brain, Behavior and Metabolism (CBBM)

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10.1016/j.brainres.2012.08.046

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title = "Connexin 36 promotes cortical spreading depolarization and ischemic brain damage",

abstract = "Cortical spreading depolarization (CSD) promotes the progression of neuronal injury after cerebral ischemia. However, the mechanisms of propagation of postischemic CSD events are still unclear. In this study we characterized the role of the main neuronal gap junction protein connexin 36 (Cx36) in generating postischemic CSDs. In Cx36-deficient mice and controls we occluded the distal middle cerebral artery. To detect CSD events we recorded the direct current and laser Doppler flow. In addition, locomotor function and the infarct size were determined. Cx36-deficient mice had significantly fewer and shorter CSD events than wild-type controls. Additionally, Cx36 deletion is neuroprotective, leading to a better functional outcome and decreased infarct size after ischemia. These results suggest a detrimental role for Cx36 after ischemia, possibly by promoting CSD.",

author = "Panagiotis Bargiotas and Sajjad Muhammad and Mahbubur Rahman and Nurith Jakob and Raimund Trabold and Elke Fuchs and Lothar Schilling and Nikolaus Plesnila and Hannah Monyer and Markus Schwaninger",

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AU - Bargiotas, Panagiotis

AU - Muhammad, Sajjad

AU - Rahman, Mahbubur

AU - Jakob, Nurith

AU - Trabold, Raimund

AU - Fuchs, Elke

AU - Schilling, Lothar

AU - Plesnila, Nikolaus

AU - Monyer, Hannah

AU - Schwaninger, Markus

PY - 2012/10/15

Y1 - 2012/10/15

N2 - Cortical spreading depolarization (CSD) promotes the progression of neuronal injury after cerebral ischemia. However, the mechanisms of propagation of postischemic CSD events are still unclear. In this study we characterized the role of the main neuronal gap junction protein connexin 36 (Cx36) in generating postischemic CSDs. In Cx36-deficient mice and controls we occluded the distal middle cerebral artery. To detect CSD events we recorded the direct current and laser Doppler flow. In addition, locomotor function and the infarct size were determined. Cx36-deficient mice had significantly fewer and shorter CSD events than wild-type controls. Additionally, Cx36 deletion is neuroprotective, leading to a better functional outcome and decreased infarct size after ischemia. These results suggest a detrimental role for Cx36 after ischemia, possibly by promoting CSD.

AB - Cortical spreading depolarization (CSD) promotes the progression of neuronal injury after cerebral ischemia. However, the mechanisms of propagation of postischemic CSD events are still unclear. In this study we characterized the role of the main neuronal gap junction protein connexin 36 (Cx36) in generating postischemic CSDs. In Cx36-deficient mice and controls we occluded the distal middle cerebral artery. To detect CSD events we recorded the direct current and laser Doppler flow. In addition, locomotor function and the infarct size were determined. Cx36-deficient mice had significantly fewer and shorter CSD events than wild-type controls. Additionally, Cx36 deletion is neuroprotective, leading to a better functional outcome and decreased infarct size after ischemia. These results suggest a detrimental role for Cx36 after ischemia, possibly by promoting CSD.

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ER -

Connexin 36 promotes cortical spreading depolarization and ischemic brain damage

Abstract

Funding

UN SDGs

Research Areas and Centers

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