Literature DB >> 27052838

Uncoupling of neurovascular communication after transient global cerebral ischemia is caused by impaired parenchymal smooth muscle Kir channel function.

Gro Klitgaard Povlsen1, Thomas A Longden2, Adrian D Bonev2, David C Hill-Eubanks, Mark T Nelson3.   

Abstract

Transient global cerebral ischemia is often followed by delayed disturbances of cerebral blood flow, contributing to neuronal injury. The pathophysiological processes underlying such disturbances are incompletely understood. Here, using an established model of transient global cerebral ischemia, we identify dramatically impaired neurovascular coupling following ischemia. This impairment results from the loss of functional inward rectifier potassium (KIR) channels in the smooth muscle of parenchymal arterioles. Therapeutic strategies aimed at protecting or restoring cerebrovascular KIR channel function may therefore improve outcomes following ischemia.
© The Author(s) 2016.

Entities:  

Keywords:  KIR channel; Neurovascular coupling; cerebral blood flow; ischemia; smooth muscle

Mesh：

Substances：

Year:  2016        PMID： 27052838      PMCID： PMC4929704          DOI： 10.1177/0271678X16638350

Source DB:  PubMed          Journal:  J Cereb Blood Flow Metab        ISSN： 0271-678X            Impact factor:   6.200


  34 in total

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Review 5.  Functional hyperemia in the brain: hypothesis for astrocyte-derived vasodilator metabolites.

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6.  Distribution of rSlo Ca2+-activated K+ channels in rat astrocyte perivascular endfeet.

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Review 7.  Physiological role of inward rectifier K(+) channels in vascular smooth muscle cells.

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Review 8.  Cerebral ischemia: models, methods and outcomes.

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  12 in total

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6.  Impaired capillary-to-arteriolar electrical signaling after traumatic brain injury.

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8.  Differential pial and penetrating arterial responses examined by optogenetic activation of astrocytes and neurons.

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9.  PIP2 Improves Cerebral Blood Flow in a Mouse Model of Alzheimer's Disease.

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10.  Cerebrovascular function and mitochondrial bioenergetics after ischemia-reperfusion in male rats.

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