Linked Life Data

14999075

Source:http://linkedlifedata.com/resource/pubmed/id/14999075

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
9
pubmed:dateCreated
2004-3-4
pubmed:abstractText
Fibroblast growth factor receptor (FGFR) gene products (Fgfr1, Fgfr2, Fgfr3) are widely expressed by embryonic neural progenitor cells throughout the CNS, yet their functional role in cerebral cortical development is still unclear. To understand whether the FGF pathways play a role in cortical development, we attenuated FGFR signaling by expressing a tyrosine kinase domain-deficient Fgfr1 (tFgfr1) gene construct during embryonic brain development. Mice carrying the tFgfr1 transgene under the control of the Otx1 gene promoter have decreased thickness of the cerebral cortex in frontal and temporal areas because of decreased number of pyramidal neurons and disorganization of pyramidal cell dendritic architecture. These alterations may be, in part, attributable to decreased genesis of T-Brain-1-positive early glutamatergic neurons and, in part, to a failure to maintain radial glia fibers in medial prefrontal and temporal areas of the cortical plate. No changes were detected in cortical GABAergic interneurons, including Cajal-Retzius cells or in the basal ganglia. Behaviorally, tFgfr1 transgenic mice displayed spontaneous and persistent locomotor hyperactivity that apparently was not attributable to alterations in subcortical monoaminergic systems, because transgenic animals responded to both amphetamine and guanfacine, an alpha2A adrenergic receptor agonist. We conclude that FGF tyrosine kinase signaling may be required for the genesis and growth of pyramidal neurons in frontal and temporal cortical areas, and that alterations in cortical development attributable to disrupted FGF signaling are critical for the inhibitory regulation of motor behavior.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Mar
pubmed:issn
1529-2401
pubmed:author
pubmed:issnType
Electronic
pubmed:day
3
pubmed:volume
24
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
2247-58
pubmed:dateRevised
2010-5-26
pubmed:meshHeading
pubmed-meshheading:14999075-Adrenergic alpha-Agonists, pubmed-meshheading:14999075-Amphetamine, pubmed-meshheading:14999075-Animals, pubmed-meshheading:14999075-Cell Differentiation, pubmed-meshheading:14999075-Cell Division, pubmed-meshheading:14999075-Frontal Lobe, pubmed-meshheading:14999075-Glutamic Acid, pubmed-meshheading:14999075-Guanfacine, pubmed-meshheading:14999075-Humans, pubmed-meshheading:14999075-Hyperkinesis, pubmed-meshheading:14999075-Mice, pubmed-meshheading:14999075-Mice, Transgenic, pubmed-meshheading:14999075-Nervous System Malformations, pubmed-meshheading:14999075-Neural Inhibition, pubmed-meshheading:14999075-Pyramidal Cells, pubmed-meshheading:14999075-Receptor, Fibroblast Growth Factor, Type 1, pubmed-meshheading:14999075-Receptor Protein-Tyrosine Kinases, pubmed-meshheading:14999075-Receptors, Adrenergic, alpha-2, pubmed-meshheading:14999075-Receptors, Fibroblast Growth Factor, pubmed-meshheading:14999075-Signal Transduction, pubmed-meshheading:14999075-Stereotypic Movement Disorder, pubmed-meshheading:14999075-Temporal Lobe
pubmed:year
2004
pubmed:articleTitle
Loss of glutamatergic pyramidal neurons in frontal and temporal cortex resulting from attenuation of FGFR1 signaling is associated with spontaneous hyperactivity in mice.
pubmed:affiliation
Child Study Center, Yale University, New Haven, Connecticut 06520, USA.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Research Support, U.S. Gov't, Non-P.H.S., Research Support, Non-U.S. Gov't