Linked Life Data

16855101

Source:http://linkedlifedata.com/resource/pubmed/id/16855101

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
29
pubmed:dateCreated
2006-7-20
pubmed:abstractText
Brain function is usually perceived as being performed by neurons with the support of glial cells, the network of blood vessels situated nearby serving simply to provide nutrient and to dispose of metabolic waste. Revising this view, we find from experiments on a rodent central white matter tract (the optic nerve) in vitro that microvascular endothelial cells signal persistently to axons using nitric oxide (NO) derived from the endothelial NO synthase (eNOS). The endogenous NO acts to stimulate guanylyl cyclase-coupled NO receptors in the axons, leading to a raised cGMP level which then causes membrane depolarization, apparently by directly engaging hyperpolarization-activated cyclic nucleotide-gated ion channels. The tonic depolarization and associated endogenous NO-dependent cGMP generation was absent in optic nerves from mice lacking eNOS, although such nerves responded to exogenous NO, with raised cGMP generation in the axons and associated depolarization. In addition to the tonic activity, exposure of optic nerves to bradykinin, a classical stimulator of eNOS in endothelial cells, elicited reversible NO- and cGMP-dependent depolarization through activation of bradykinin B2 receptors, to which eNOS is physically complexed. No contribution of other NO synthase isoforms to either the action of bradykinin or the continuous ambient NO level could be detected. The results suggest that microvascular endothelial cells participate in signal processing in the brain and can do so by generating both tonic and phasic NO signals.
pubmed:grant
pubmed:commentsCorrections
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jul
pubmed:issn
1529-2401
pubmed:author
pubmed:issnType
Electronic
pubmed:day
19
pubmed:volume
26
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
7730-40
pubmed:dateRevised
2007-11-15
pubmed:meshHeading
pubmed-meshheading:16855101-Animals, pubmed-meshheading:16855101-Blood Vessels, pubmed-meshheading:16855101-Bradykinin, pubmed-meshheading:16855101-Brain, pubmed-meshheading:16855101-Cyclic GMP, pubmed-meshheading:16855101-Cyclic Nucleotide-Gated Cation Channels, pubmed-meshheading:16855101-Electrophysiology, pubmed-meshheading:16855101-Endothelial Cells, pubmed-meshheading:16855101-Ion Channels, pubmed-meshheading:16855101-Isoenzymes, pubmed-meshheading:16855101-Mice, pubmed-meshheading:16855101-Mice, Inbred Strains, pubmed-meshheading:16855101-Mice, Knockout, pubmed-meshheading:16855101-Microcirculation, pubmed-meshheading:16855101-Nitric Oxide, pubmed-meshheading:16855101-Nitric Oxide Synthase, pubmed-meshheading:16855101-Nitric Oxide Synthase Type III, pubmed-meshheading:16855101-Optic Nerve, pubmed-meshheading:16855101-Potassium Channels, pubmed-meshheading:16855101-Rats, pubmed-meshheading:16855101-Signal Transduction
pubmed:year
2006
pubmed:articleTitle
Signaling from blood vessels to CNS axons through nitric oxide.
pubmed:affiliation
Wolfson Institute for Biomedical Research, University College London, London WC1E 6BT, United Kingdom. g.garthwaite@ucl.ac.uk
pubmed:publicationType
Journal Article, In Vitro, Research Support, Non-U.S. Gov't