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This Article Full Text Full Text (PDF) All Versions of this Article: 92/4/641    most recent expphysiol.2006.036368v1 Alert me when this article is cited Alert me if a correction is posted Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via Google Scholar Google Scholar Articles by Filosa, J. A. Articles by Blanco, V. M. Search for Related Content PubMed PubMed Citation Articles by Filosa, J. A. Articles by Blanco, V. M. Related Collections Vascular

¹ Department of Psychiatry, University of Cincinnati, 2170 East Galbraith Road, Room 239-A, Cincinnati, OH 45237, USA

Abstract

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 studies. In this article, we discuss the various astrocyte-derived vasodilating and vasoconstricting signals, their interactions and effects on astrocytes and vascular smooth muscle cells, and suggest the importance of the intrinsic properties of the latter cell type on the overall neurovascular response. We present a working model in which the 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. We 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.

(Received 16 March 2007; accepted after revision 4 May 2007; first published online 4 May 2007)
Corresponding author J. A. Filosa: Department of Psychiatry, University of Cincinnati, 2170 East Galbraith Road, Room 239-A, Cincinnati, OH 45237, USA. Email: jessica.filosa{at}uc.edu