What is the logical conclusion after this research and what theory can be tested to help survivors?
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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