Experimental Physiology 92.4 pp 641-646DOI: 10.1113/expphysiol.2006.036368Jessica A. Filosa1 and Víctor M. Blanco11 Department of Psychiatry, University of Cincinnati, 2170 East Galbraith Road, Room 239-A, Cincinnati, OH 45237, USA
Normal brain function requires proper supply of oxygen and glucose in a timely and local manner. This is achieved through an orchestrated intercellular communication between neurones, astrocytes and microvessels that results in a rapid and restricted increase in cerebral blood flow, a process known as neurovascular coupling. Astrocytic end-feet make close contacts with neuronal synapses and blood vessels and, given their ability to release vasoactive signals following neuronal activation, have been recognized as key intermediaries in the neurovascular response. Both dilating and constricting signals appear to be released from astrocytes upon increases in intracellular Ca2+ concentration, and both dilatation and constriction of brain vessels have been observed in previous studiesthe rise in astrocytic Ca2+ following neuronal activation leads not only to the rapid activation of calcium-activated K+ channels in astrocytic end-feet, but also to their modulation by metabolites of the arachidonic acid pathway, which in general have been proposed to act on vascular smooth muscle cells rather than on astrocytes. They propose that this latter mechanism may in turn modulate K+ signalling from astrocytes to smooth muscle cells, influencing the overall effects of the vasodilating and vasoconstricting signals released during neuronal activation.
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