Linked Life Data

21434925

Source:http://linkedlifedata.com/resource/pubmed/id/21434925

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
5
pubmed:dateCreated
2011-5-5
pubmed:abstractText
Dehydroepiandrosterone (DHEA) is one of the most abundant neurosteroids synthesized de novo in the CNS. We here found that sigma-1 receptor stimulation by DHEA improves cognitive function through phosphorylation of synaptic proteins in olfactory bulbectomized (OBX) mouse hippocampus. We have previously reported that calcium/calmodulin-dependent protein kinase II (CaMKII), protein kinase C (PKC) and extracellular signal-regulated kinase (ERK) were impaired in OBX mouse hippocampus. OBX mice were administered once a day for 7-8 days with DHEA (30 or 60 mg/kg p.o.) 10 days after operation. The spatial, cognitive and conditioned fear memories in OBX mice were significantly improved as assessed by Y-maze, novel object recognition and passive avoidance task, respectively. DHEA also improved impaired hippocampal long-term potentiation in OBX mice. Notably, DHEA treatment restored PKC? (Ser-657) autophosphorylation and NR1 (Ser-896) and myristoylated alanine-rich protein kinase C substrate (Ser-152/156) phosphorylation to the control levels in the hippocampal CA1 region. Likewise, DHEA treatment improved CaMKII? (Thr-286) autophosphorylation and GluR1 (Ser-831) phosphorylation to the control levels in the CA1 region. Furthermore, DHEA treatment improved ERK and cAMP-responsive element-binding protein (Ser-133) phosphorylation to the control levels. Finally, NE-100, sigma-1 receptor antagonist, significantly inhibited the DHEA-induced improvement of memory-related behaviors and CaMKII, PKC and ERK phosphorylation in CA1 region. Taken together, sigma-1 receptor stimulation by DHEA ameliorates OBX-induced impairment in memory-related behaviors and long-term potentiation in the hippocampal CA1 region through activation of CaMKII, PKC and ERK.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jun
pubmed:issn
1471-4159
pubmed:author
pubmed:copyrightInfo
© 2011 The Authors. Journal of Neurochemistry © 2011 International Society for Neurochemistry.
pubmed:issnType
Electronic
pubmed:volume
117
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
879-91
pubmed:meshHeading
pubmed-meshheading:21434925-Animals, pubmed-meshheading:21434925-Anisoles, pubmed-meshheading:21434925-Avoidance Learning, pubmed-meshheading:21434925-Behavior, Animal, pubmed-meshheading:21434925-Blotting, Western, pubmed-meshheading:21434925-CA1 Region, Hippocampal, pubmed-meshheading:21434925-Calcium-Calmodulin-Dependent Protein Kinase Type 2, pubmed-meshheading:21434925-Cognition Disorders, pubmed-meshheading:21434925-Dehydroepiandrosterone, pubmed-meshheading:21434925-Electrophysiological Phenomena, pubmed-meshheading:21434925-Enzyme Activation, pubmed-meshheading:21434925-Extracellular Signal-Regulated MAP Kinases, pubmed-meshheading:21434925-Hippocampus, pubmed-meshheading:21434925-Long-Term Potentiation, pubmed-meshheading:21434925-Male, pubmed-meshheading:21434925-Maze Learning, pubmed-meshheading:21434925-Memory Disorders, pubmed-meshheading:21434925-Mice, pubmed-meshheading:21434925-Olfactory Bulb, pubmed-meshheading:21434925-Phosphorylation, pubmed-meshheading:21434925-Propylamines, pubmed-meshheading:21434925-Protein Kinase C, pubmed-meshheading:21434925-Psychomotor Performance, pubmed-meshheading:21434925-Receptors, sigma, pubmed-meshheading:21434925-Recognition (Psychology)
pubmed:year
2011
pubmed:articleTitle
Sigma-1 receptor stimulation by dehydroepiandrosterone ameliorates cognitive impairment through activation of CaM kinase II, protein kinase C and extracellular signal-regulated kinase in olfactory bulbectomized mice.
pubmed:affiliation
Department of Pharmacology, Graduate School of Pharmaceutical Sciences, Tohoku University, 6-3 Aramaki-Aoba, Sendai, Japan.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't