Received March 16, 2007
Revised April 16, 2007
Accepted after revision May 4, 2007
Neurovascular communication in the brain
Jessica A Filosa 1*
Victor M Blanco 1
1 University of Cincinnati
* To whom correspondence should be addressed. E-mail: jessica.filosa{at}uc.edu.
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Abstract |
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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 neurons, astrocytes and
microvessels that results in a rapid and restricted
increase in cerebral blood flow, a process known as
neurovascular coupling. Astrocytic endfeet 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 [Ca2+]
i, and both dilation and constriction of
brain vessels have been subsequently 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 where the rise in astrocytic
Ca2+ following neuronal activation leads not
only to the rapid activation of calcium-activated
K+ channels in astrocytic endfeet, 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+ signaling from astrocytes
to smooth muscle cells, influencing the overall effects
of the vasodilating and vasoconstricting signals
released during neuronal activation.
Key Words:
Calcium, Glia, Potassium channel
