Linked Life Data

15530873

Source:http://linkedlifedata.com/resource/pubmed/id/15530873

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
2
pubmed:dateCreated
2004-11-8
pubmed:abstractText
Brain-derived neurotrophic factor (BDNF) acts through the neurotrophin receptor TrkB and promotes survival and differentiation of dopaminergic ventral mesencephalic neurons. To further evaluate the role of TrkB in the nigrostriatal pathway, we studied neurotrophin levels, dopamine metabolism, and morphology of dopaminergic neurons of the substantia nigra (SN-DA) in young adult hypomorphic trkB mice (trkBfbz/fbz), which express only approximately 25% of wild type levels of TrkB. Tyrosine hydroxylase immunostaining revealed altered morphology of SN-DA neurons in trkBfbz/fbz when compared to wild type mice, in particular a significant enlargement of nuclear size. Cell counts revealed a pronounced loss of SN-DA neurons in these mice. Measurement of monoamine levels by high performance liquid chromatography (HPLC) showed that dopamine (DA) levels in the target field (striatum) were significantly elevated in trkBfbz/fbz compared to trkB+/fbz and wild type mice (P < 0.05), without altering DA turnover. Likewise, enzyme-linked immunosorbent assay (ELISA) for neurotrophic factors measurement showed that BDNF levels were increased in the striatum (P < 0.01) and frontal cortex (P < 0.005) of trkBfbz/fbz mice, but not in the SN when compared to trkB+/fbz and wild type mice. These data suggest that elevated neurotransmitter and neurotrophic factor levels might be a compensatory mechanism following dopaminergic cell loss in the SN. Thus, TrkB-activation seems essential for the maintenance of the nigrostriatal dopaminergic system.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Dec
pubmed:issn
0014-4886
pubmed:author
pubmed:issnType
Print
pubmed:volume
190
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
337-46
pubmed:dateRevised
2009-11-19
pubmed:meshHeading
pubmed-meshheading:15530873-3,4-Dihydroxyphenylacetic Acid, pubmed-meshheading:15530873-Animals, pubmed-meshheading:15530873-Brain-Derived Neurotrophic Factor, pubmed-meshheading:15530873-Chromatography, High Pressure Liquid, pubmed-meshheading:15530873-Corpus Striatum, pubmed-meshheading:15530873-Dopamine, pubmed-meshheading:15530873-Enzyme-Linked Immunosorbent Assay, pubmed-meshheading:15530873-Frontal Lobe, pubmed-meshheading:15530873-Homovanillic Acid, pubmed-meshheading:15530873-Immunohistochemistry, pubmed-meshheading:15530873-Mice, pubmed-meshheading:15530873-Mice, Transgenic, pubmed-meshheading:15530873-Nerve Degeneration, pubmed-meshheading:15530873-Neurons, pubmed-meshheading:15530873-Receptor, trkA, pubmed-meshheading:15530873-Substantia Nigra, pubmed-meshheading:15530873-Tyrosine 3-Monooxygenase
pubmed:year
2004
pubmed:articleTitle
Neurodegenerative alterations in the nigrostriatal system of trkB hypomorphic mice.
pubmed:affiliation
Department of Physiology and Neuroscience, Medical University of South Carolina, Charleston, SC 29425, USA. zamanv@musc.edu
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Research Support, U.S. Gov't, Non-P.H.S.