Linked Life Data

19345723

Source:http://linkedlifedata.com/resource/pubmed/id/19345723

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
3
pubmed:dateCreated
2009-6-1
pubmed:abstractText
The glial cell water channel aquaporin-4 (AQP4) plays an important role in brain edema, astrocyte migration, and neuronal excitability. Zhou et al. [Zhou J, Kong H, Hua X, Xiao M, Ding J, Hu G (2008) Altered blood-brain barrier integrity in adult aquaporin-4 knockout mice. Neuroreport 19:1-5] recently reported that AQP4 deletion significantly altered blood-brain barrier integrity and glial fibrillary acidic protein (GFAP) immunoreactivity in their AQP4 null mice. Here we describe a detailed characterization of baseline brain properties in our AQP4 null mice, including gross appearance, neuronal, astrocyte and oligodendrocyte characteristics, and blood-brain barrier integrity. Gross anatomical measurements included estimates of brain and ventricle size. Neurons, astrocytes and oligodendrocytes were assessed using the neuronal nuclear marker NeuN, the astrocyte marker GFAP, and the myelin stain Luxol Fast Blue. The blood-brain barrier was studied by electron microscopy and the horseradish peroxidase extravasation technique. There were no differences in brain and ventricle sizes between wild type and AQP4 null mice, nor were there differences in the cerebral cortical density of NeuN positive nuclei, perimicrovessel and glia limitans GFAP immunoreactivity, or the thickness and myelination of the corpus callosum. The ultrastructure of microvessels in the frontal cortex and caudate nucleus of wild type vs. AQP4 null mice was indistinguishable, with features including intact endothelial tight junctions, absence of perimicrovessel astrocyte foot process edema, and absence of horseradish peroxidase extravasation. In contrast to the report by Zhou et al. (2008), our data show that AQP4 deletion in mice does not produce major structural abnormalities in the brain.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jul
pubmed:issn
1873-7544
pubmed:author
pubmed:issnType
Electronic
pubmed:day
7
pubmed:volume
161
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
764-72
pubmed:meshHeading
pubmed-meshheading:19345723-Animals, pubmed-meshheading:19345723-Aquaporin 4, pubmed-meshheading:19345723-Astrocytes, pubmed-meshheading:19345723-Blood-Brain Barrier, pubmed-meshheading:19345723-Brain, pubmed-meshheading:19345723-Cerebral Ventricles, pubmed-meshheading:19345723-Gene Deletion, pubmed-meshheading:19345723-Horseradish Peroxidase, pubmed-meshheading:19345723-Indoles, pubmed-meshheading:19345723-Male, pubmed-meshheading:19345723-Mice, pubmed-meshheading:19345723-Mice, Knockout, pubmed-meshheading:19345723-Microvessels, pubmed-meshheading:19345723-Nerve Fibers, Myelinated, pubmed-meshheading:19345723-Nerve Tissue Proteins, pubmed-meshheading:19345723-Neurons, pubmed-meshheading:19345723-Nuclear Proteins, pubmed-meshheading:19345723-Oligodendroglia, pubmed-meshheading:19345723-Organ Size
pubmed:year
2009
pubmed:articleTitle
AQP4 gene deletion in mice does not alter blood-brain barrier integrity or brain morphology.
pubmed:affiliation
Academic Neurosurgery Unit, St. George's, University of London, London, UK.
pubmed:publicationType
Journal Article, Review, Research Support, Non-U.S. Gov't