Journal
CURRENT PHARMACEUTICAL DESIGN
Volume 23, Issue 33, Pages 5056-5074Publisher
BENTHAM SCIENCE PUBL LTD
DOI: 10.2174/1381612823666170710161858
Keywords
Reactive astrocytes; potassium buffering; glutamate homeostasis; ion channels; transporters; brain ischemia
Categories
Funding
- Grant agency of the Czech Republic [GA CR 15-02760S, GA CR 16-10214S]
Ask authors/readers for more resources
Brain ischemic injury represents one of the greatest medical challenges for the aging population in developed countries, yet despite strong efforts, possibilities to treat ischemic injury still remain poor. Stroke, the most common type of brain ischemic injury in humans, is caused by brain artery occlusion, and represents a focal form of ischemia, which leads to neuronal loss in the ischemic core, and glial scar formation in the penumbral region around the core. Such glial scar mainly comprises reactive astrocytes, reactive NG2 glia and activated microglia. Reactive astrocytes display distinct features when compared to healthy astroglia, including changes in their morphology, metabolism, gene expression profiles, production of extracellular matrix proteins or proliferation rate. Similarly to astrocytes in the healthy nervous tissue, reactive astrocytes surrounding the glial scar strongly influence the activity of surviving neurons around the ischemic lesion. Bringing insight into pathophysiological functions of reactive astrocytes within the glial scar might thus open new possibilities for stroke treatment. Here, we summarize the properties of reactive astrocytes, with emphasis on the expression and function of ion channels, transporters and neurotransmitter receptors; all of which possess the ability to change the functional state of astrocytes, such as the membrane equilibrium potentials for different ions. This may have major effects on the functioning of surviving neurons, consequently leading to changes in neuronal excitability and progression of secondary pathologies, such as epilepsy. Moreover, we provide possible clues for therapy, based on functional modulation of astrocytic ion transporting mechanisms.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available