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Symposium Reports |
1 Department of Psychiatry, University of Cincinnati, 2170 East Galbraith Road, Room 239-A, Cincinnati, OH 45237, USA
Email: jessica.filosa{at}uc.edu
This issue contains four papers based on a symposium entitled Neural–Glial–Vascular Communication in the Brain, which took place at the Experimental Biology meeting in Washington, DC, USA, 29th April 2007.
Over a century ago, seminal investigations revealed that brain activity was tightly associated with an increase in blood flow (Mosso, 1880; Roy & Sherrington, 1890), a phenomenon known today as functional hyperaemia. Since then, enormous efforts have focused on understanding the cellular mechanism underlying functional hyperaemia in the brain. It is now clear that rapid increases in blood flow in response to neuronal activation require an exquisite organization involving multiple cell types and signals, a process also referred to as ‘neurovascular coupling’. Recent findings have demonstrated the importance of various signals derived from neuronal and glial sources in translating the state of neuronal activity to dynamic alterations in the nearby microcirculation. The purpose of the ‘Neural–Glial–Vascular Communication in the Brain’ symposium was to provide an update on some of the most recent findings addressing the nature of the neurovascular response and the potential mechanisms mediating this orchestrated phenomenon. The following four reports summarize the topics addressed by the speakers during the symposium.
Dr E. Newman discussed the involvement of K+ siphoning, metabolites of the arachidonic acid pathway and nitric oxide in the signalling mechanisms underlying neurovascular coupling in the retina (Metea & Newman, 2007). Dr J. Filosa addressed current evidence supporting a role for K+ signalling between astrocytic end-feet and vascular smooth muscle cells and described the changes in intracellular Ca2+ that occur in both cell types during vascular responses in the brain microcirculation (Filosa & Blanco, 2007). Dr D. Pelligrino presented new findings addressing the importance of purinergic mechanisms involving ATP release and hydrolysis, with emphasis on the signalling events underlying the communication between the glial limitans and pial arterioles (Xu & Pelligrino, 2007). Finally, J. Iliff provided evidence for the expression of a P450 epoxygenase isoform (CYP2C11) and of soluble epoxide hydrolase in extrinsic parasympathetic and sensory vasodilatory nerve fibres contacting the middle cerebral artery and proposed a novel role for P450 eicosanoids in the neurovascular control of the cerebral circulation (Iliff et al. 2007). Altogether, these reports add new impetus to this exciting area of research and highlight the complexity of the neurovascular response in the brain.
This symposium was kindly sponsored by the Central Nervous System Section of the American Physiological Society.
References
Filosa JA & Blanco VM (2007). Neurovascular coupling in the mammalian brain. Exp Physiol 92, 641–646.
Iliff JJ, Close LN, Selden NR & Alkayed NJ (2007). A novel role for P450 eicosanoids in the neurogenic control of cerebral blood flow. Exp Physiol 92, 653–658.
Metea MR & Newman EA (2007). Signaling within the neurovascular unit in the mammalian retina. Exp Physiol 92, 635–640.
Mosso A (1880). Sulla circolazione del cervello dell'uomo. Atti R Accad Lincei 5, 237–358.
Roy CS & Sherrington C (1890). On the regulation of the blood supply of the brain. J Physiol 11, 85–108.
Xu H-L & Pelligrino DA (2007). ATP release and hydrolysis contributes to mammalian pial arteriolar dilatation elicited by neuronal activation. Exp Physiol 92, 647–651.
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