Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
8
pubmed:dateCreated
2010-4-22
pubmed:abstractText
Intracerebroventricular injection of beta-amyloid(25-35) (Abeta(25-35)) in mice leads to cognitive deficits with the dysfunction of alpha7 nicotinic acetylcholine receptor (alpha7nAChR) within 1-2 weeks in a dose-dependent manner. The present study focused on the effect of DMXB, a selective alpha7nAChR agonist, on Abeta(25-35) (3 nmol)-impaired spatial memory and alpha7nAChR function. We found that the treatment with DMXB on days 1-10 after Abeta(25-35) injection dose-dependently prevented Abeta(25-35)-induced impairment of acquisition performance and probe trail test in Morris water maze. Importantly, the treatment with DMXB (1 mg/kg) perfectly prevented Abeta(25-35)-induced depression of alpha7nAChR response, which was associated with improving the probability of presynaptic glutamate release and the induction of high-frequency stimulation (HFS)-dependent long-term potentiation (LTP) in hippocampal Schaffer collaterale-CA1 synapse. Furthermore, although either the basal level of extracellular signal-regulated kinase 2 (ERK2) or its phosphorylation in the hippocampus had no difference between control and Abeta(25-35) mice, the Abeta(25-35) injection significantly attenuated HFS-triggered increase in ERK2 phosphorylation. The treatment with DMXB also rescued the ERK2 phosphorylation triggered by HFS in Abeta(25-35) mice that is required for LTP induction. This study firstly provides in vivo evidence that the anti-amnesic effect of DMXB is likely due to preventing the Abeta(25-35)-induced dysfunction of alpha7nAChR.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jun
pubmed:issn
1097-4547
pubmed:author
pubmed:issnType
Electronic
pubmed:volume
88
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
1784-94
pubmed:dateRevised
2010-11-18
pubmed:meshHeading
pubmed-meshheading:20127813-Amyloid beta-Peptides, pubmed-meshheading:20127813-Animals, pubmed-meshheading:20127813-Behavior, Animal, pubmed-meshheading:20127813-Benzylidene Compounds, pubmed-meshheading:20127813-Cognition Disorders, pubmed-meshheading:20127813-Disease Models, Animal, pubmed-meshheading:20127813-Dose-Response Relationship, Drug, pubmed-meshheading:20127813-Drug Interactions, pubmed-meshheading:20127813-Electric Stimulation, pubmed-meshheading:20127813-Evoked Potentials, pubmed-meshheading:20127813-Gene Expression Regulation, pubmed-meshheading:20127813-Hippocampus, pubmed-meshheading:20127813-Male, pubmed-meshheading:20127813-Maze Learning, pubmed-meshheading:20127813-Mice, pubmed-meshheading:20127813-Mice, Inbred ICR, pubmed-meshheading:20127813-Mitogen-Activated Protein Kinase 1, pubmed-meshheading:20127813-Neuronal Plasticity, pubmed-meshheading:20127813-Nicotinic Agonists, pubmed-meshheading:20127813-Peptide Fragments, pubmed-meshheading:20127813-Phosphorylation, pubmed-meshheading:20127813-Pyridines, pubmed-meshheading:20127813-Reaction Time, pubmed-meshheading:20127813-Receptors, Nicotinic, pubmed-meshheading:20127813-Space Perception
pubmed:year
2010
pubmed:articleTitle
DMXB (GTS-21) ameliorates the cognitive deficits in beta amyloid(25-35(-) ) injected mice through preventing the dysfunction of alpha7 nicotinic receptor.
pubmed:affiliation
Department of Physiology, Nanjing Medical University, Nanjing, China.
pubmed:publicationType
Journal Article, In Vitro, Research Support, Non-U.S. Gov't