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Bidirectional control of arteriole diameter by astrocytes
Author(s) -
Gordon Grant R. J.,
Howarth Clare,
MacVicar Brian A.
Publication year - 2011
Publication title -
experimental physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.925
H-Index - 101
eISSN - 1469-445X
pISSN - 0958-0670
DOI - 10.1113/expphysiol.2010.053132
Subject(s) - biology , astrocyte , arachidonic acid , phospholipase a2 , vascular smooth muscle , metabotropic glutamate receptor , microbiology and biotechnology , vasodilation , medicine , endocrinology , nitric oxide , neurotransmission , glutamate receptor , biochemistry , receptor , central nervous system , smooth muscle , enzyme
Astrocytes are the most numerous cells in the CNS. It is a defining feature of brain anatomy that every astrocyte has at least one contact with the vasculature, termed an endfoot. Collectively, all endfeet completely circumscribe all vessels in the brain. This unique anatomical feature has profound functional significance, as astrocyte endfeet have been discovered to release diffusible messengers that communicate directly with underlying smooth muscle cells to change arterial diameter and thereby regulate cerebral blood flow. A growing body of data now demonstrates that astrocytes serve as a bridge, relaying information on the level of neural activity to blood vessels in order to co‐ordinate oxygen and glucose delivery with the energy demands of the tissue. In particular, astrocytes respond to elevations in extracellular glutamate as a consequence of synaptic transmission through the activation of group 1 metabotropic glutamate receptors. These Gq‐coupled receptors elevate intracellular calcium via IP 3 signalling, which activates phospholipase A2 and generates arachidonic acid. Arachidonic acid acts as a signalling molecule or is converted to several lipid derivates, including prostaglandin E 2 and epoxyeicosatrienoic acids. Each of these lipids acts on vascular smooth muscle cells via different mechanisms to affect vessel diameter. Arachidonic acid initiates the production of 20‐hydroxyeicosatetraenoic acid to cause vasoconstriction, whereas prostaglandin E 2 and epoxyeicosatrienoic acids cause vasodilatation. Factors that determine whether constrictor or dilatory pathways predominate involve nitric oxide and brain metabolic elements, such as oxygen, lactate and adenosine. Thus, astrocytes are thought to be capable of bidirectional control of arterial diameter, and the type of influence depends on the state of brain activity.