Received March 21, 2007
Revised April 13, 2007
Accepted after revision April 24, 2007
ATP release and hydrolysis contributes to pial arteriolar
dilations elicited by neuronal activation
Hao-Liang Xu 1*
Dale A. Pelligrino 1
1 University of Illinois at Chicago
* To whom correspondence should be addressed. E-mail: hlxu{at}uic.edu.
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Abstract |
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Because of their intimate anatomic relationship with cerebral arterioles, astrocytes have been postulated as signal transducers, transferring information from activated neurons to the cerebral microcirculation. These forwarded signals may involve the release of vasoactive factors from the endfeet of astrocytes. The above is labeled as "neurovascular coupling" and its components (i.e., neuron, astrocyte, and vascular cells) as the "neurovascular unit"The process of neurovascular coupling often involves upstream dilation. This is necessary during periods of increased metabolic demand, in order to permit more blood to reach dilated downstream vessels, thereby improving nutrient supply to the activated neurons. Without it, that downstream dilation may be ineffective, placing neurons at risk, especially during episodes of intense neuronal activity, such as seizure. In the brain, pial arterioles represent important "upstream" vascular segments. The pial arterioles overlie a thick layer of astrocytic processes, termed glia limitans. This essentially isolates pial arterioles, anatomically, from the neurons below. Vasodilating signals, originating in the neurons, therefore, reach the pial arterioles via indirect pathways, primarily involving astrocytes and the glia limitans. Here we discuss a process whereby purinergic mechanisms play a key and neuronal activity-dependent role in asytocyte-to-astrocyte communication, as well as glia limitans to pial arteriolar signals leading to vasodilation.
Key Words:
Adenosine, Brain, Vasodilatation
