Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1
pubmed:dateCreated
2001-7-19
pubmed:abstractText
Fibroblast growth factor 2 (FGF-2) and glial cell line-derived neurotrophic factor (GDNF) support survival of dopaminergic midbrain neurons. Neurons are coupled by gap junctions, propagating metabolites and intracellular second messengers possibly mediating growth factor effects. We asked, therefore, whether gap junctions influence the survival-promoting effects of FGF-2 and GDNF. RT-PCR, Western blotting, and immunocytochemistry demonstrate that FGF-2 but not GDNF upregulates cx43 mRNA and immunoreactivity in rat embryonic day 14 midbrain cultures, whereas cx26, cx32, and cx45 were unchanged. In addition, functional coupling as assayed by the spread of neurobiotin was increased by FGF-2. Furthermore, the gap junction blocker oleamide abolished survival-promoting effects of FGF-2 on dopaminergic midbrain neurons. Together, these results support a direct role of gap junction communication for survival-promoting effects of FGF-2 on dopaminergic midbrain neurons, making gap junction communication a substantial parameter for neuron survival.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jul
pubmed:issn
1044-7431
pubmed:author
pubmed:copyrightInfo
Copyright 2001 Academic Press.
pubmed:issnType
Print
pubmed:volume
18
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
44-55
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed:year
2001
pubmed:articleTitle
Gap junctions modulate survival-promoting effects of fibroblast growth factor-2 on cultured midbrain dopaminergic neurons.
pubmed:affiliation
Neuroanatomy and Interdisciplinary Center for Neurosciences (IZN), University of Heidelberg, Im Neuenheimer Feld 307, Heidelberg, D-69120, Germany.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't