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

7 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

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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.",

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T1 - Connexin 36 promotes cortical spreading depolarization and ischemic brain damage

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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JO - Brain Research

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Connexin 36 promotes cortical spreading depolarization and ischemic brain damage

Abstract

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