Linked Life Data

14534260

Source:http://linkedlifedata.com/resource/pubmed/id/14534260

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
27
pubmed:dateCreated
2003-10-9
pubmed:abstractText
Advances in fluorescent calcium indicating dyes over the past decade have identified calcium signaling as the tool by which astrocytes communicate among themselves and with neighboring neurons. Studies of astrocyte-neuron interactions have shown that calcium signaling is a potent modulator of the strength of both excitatory and inhibitory synapses. The concept that astrocytes possess a mechanism for rapid cell communication has not been incorporated, however, into the supportive functions of astrocytes. Because many of the classical tasks of astrocytes are linked to the blood-brain barrier, we have here examined the expression of proteins required for calcium signaling in their vascular end-foot processes. The gap junction protein, Cx43, was expressed intensively around the vessels interconnecting astrocytic end-foot processes. These gap junctions permitted diffusion of Lucifer yellow, specifically along the path of glial end feet apposed to the vessel wall. The purinergic receptors, P2Y(2) and P2Y(4), were also strongly expressed at the gliovascular interface and colocalized with GFAP around larger vessels in cortex. Multiphoton imaging of freshly prepared brain slices loaded with Fluo-4/AM revealed that ATP mobilized cytosolic calcium in astrocytic end feet, whereas electrical stimulation triggered calcium waves propagating along the vessel wall. Brain endothelial cells and pericytes were physically separated from astrocytes by the basal lamina and responded only weakly to ATP. These observations identify astrocytic end-foot processes plastered at the vessel wall as a center for purinergic signaling. It is speculated that calcium signaling may play a role in astrocytic functions related to the blood-brain barrier, including blood flow regulation, metabolic trafficking, and water homeostasis.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Oct
pubmed:issn
1529-2401
pubmed:author
pubmed:issnType
Electronic
pubmed:day
8
pubmed:volume
23
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
9254-62
pubmed:dateRevised
2010-11-18
pubmed:meshHeading
pubmed-meshheading:14534260-Adenosine Triphosphate, pubmed-meshheading:14534260-Animals, pubmed-meshheading:14534260-Astrocytes, pubmed-meshheading:14534260-Basement Membrane, pubmed-meshheading:14534260-Blood-Brain Barrier, pubmed-meshheading:14534260-Brain, pubmed-meshheading:14534260-Calcium Signaling, pubmed-meshheading:14534260-Cerebrovascular Circulation, pubmed-meshheading:14534260-Connexin 43, pubmed-meshheading:14534260-Diffusion, pubmed-meshheading:14534260-Endothelium, Vascular, pubmed-meshheading:14534260-Fluorescent Dyes, pubmed-meshheading:14534260-Gap Junctions, pubmed-meshheading:14534260-Glial Fibrillary Acidic Protein, pubmed-meshheading:14534260-Male, pubmed-meshheading:14534260-Microcirculation, pubmed-meshheading:14534260-Patch-Clamp Techniques, pubmed-meshheading:14534260-Pericytes, pubmed-meshheading:14534260-Rats, pubmed-meshheading:14534260-Rats, Sprague-Dawley, pubmed-meshheading:14534260-Receptors, Purinergic P2, pubmed-meshheading:14534260-Receptors, Purinergic P2Y2
pubmed:year
2003
pubmed:articleTitle
Signaling at the gliovascular interface.
pubmed:affiliation
Department of Neurosurgery, New York Medical College, Valhalla, New York 10590, USA.
pubmed:publicationType
Journal Article, In Vitro, Research Support, U.S. Gov't, P.H.S.