Linked Life Data

16034442

Source:http://linkedlifedata.com/resource/pubmed/id/16034442

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
2
pubmed:dateCreated
2006-1-19
pubmed:abstractText
This study is designed to characterize the signal cascades by which brain-derived neurotrophic factor (BDNF) modulates long-term memory of fear conditioning. Enzyme-linked immunosorbent assay (ELISA) and Western blot analysis of tissue homogenates taken from fear-conditioned rats showed an increase in the amygdala of BDNF protein levels and its receptor TrkB phosphorylation. Bilateral administration of a TrkB ligand scavenger TrkB IgG and a Trk-specific tyrosine kinase inhibitor K252a to the amygdala impaired fear memory, as measured with fear-potentiated startle. Fear conditioning resulted in the association of Shc and TrkB, Shc and Ras, the increase in active Ras and phosphorylation of mitogen-activated protein kinase (MAPK). Treatment of amygdala slices with BDNF for 15 min increased the levels of active Ras, and MAPK and Akt phosphorylation. BDNF-induced MAPK phosphorylation was completely abolished by MEK inhibitors, and was partially inhibited by farnesyltransferase or phosphatidylinositol-3 kinase (PI-3 kinase) inhibitors. On the other hand, BDNF-induced Akt phosphorylation was unaffected by farnesyltransferase or MEK inhibitors, but could be blocked by PI-3 kinase inhibitors. Together, these data suggest a requirement of BDNF for fear learning. The memory-enhancing effect of BDNF involves the activation of MAPK and PI-3 kinase. BDNF-induced MAPK phosphorylation in the amygdala is mediated via TrkB and the Shc-binding site. Shc binding to TrkB leads to activation of Ras, Raf, and MEK. In addition, BDNF could induce phosphorylation of MAPK via activation of PI-3 kinase.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Feb
pubmed:issn
0893-133X
pubmed:author
pubmed:issnType
Print
pubmed:volume
31
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
287-96
pubmed:dateRevised
2011-5-18
pubmed:meshHeading
pubmed-meshheading:16034442-Amygdala, pubmed-meshheading:16034442-Animals, pubmed-meshheading:16034442-Antibodies, pubmed-meshheading:16034442-Behavior, Animal, pubmed-meshheading:16034442-Blotting, Western, pubmed-meshheading:16034442-Brain-Derived Neurotrophic Factor, pubmed-meshheading:16034442-Conditioning (Psychology), pubmed-meshheading:16034442-Electroshock, pubmed-meshheading:16034442-Enzyme Inhibitors, pubmed-meshheading:16034442-Extracellular Signal-Regulated MAP Kinases, pubmed-meshheading:16034442-Fear, pubmed-meshheading:16034442-Gene Expression, pubmed-meshheading:16034442-Immunoprecipitation, pubmed-meshheading:16034442-Male, pubmed-meshheading:16034442-Monomeric GTP-Binding Proteins, pubmed-meshheading:16034442-Phosphatidylinositol 3-Kinases, pubmed-meshheading:16034442-Phosphorylation, pubmed-meshheading:16034442-Rats, pubmed-meshheading:16034442-Rats, Sprague-Dawley, pubmed-meshheading:16034442-Startle Reaction, pubmed-meshheading:16034442-Time Factors
pubmed:year
2006
pubmed:articleTitle
Regulation of amygdala-dependent learning by brain-derived neurotrophic factor is mediated by extracellular signal-regulated kinase and phosphatidylinositol-3-kinase.
pubmed:affiliation
Institute of Basic Medical Sciences and Department of Pharmacology, National Cheng-Kung University, Tainan, Taiwan, ROC.
pubmed:publicationType
Journal Article, Comparative Study, In Vitro, Research Support, Non-U.S. Gov't