Linked Life Data

17540011

Source:http://linkedlifedata.com/resource/pubmed/id/17540011

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
6
pubmed:dateCreated
2007-9-4
pubmed:abstractText
Scopolamine-treated rats are commonly used as a psychopharmacological model of memory dysfunction and have been extensively studied to establish the effectiveness of acetylcholinesterase inhibitors in the treatment of Alzheimer's disease. Scopolamine is a muscarinic acetylcholine receptor antagonist that induces memory deficits in young subjects similar to those occurring during aging. The amnesic effect of scopolamine is well established but the molecular and cellular mechanisms that sustain its neuropharmacological action are still unclear. The present genome wide study investigates hippocampal gene expression profiling in scopolamine-treated adult rats following stimulation in a spatial memory task. Using microarray and quantitative real-time RT-PCR approaches, we identified several genes previously known to be associated with memory processes (Homer1, GABA(B) receptor, early growth response 1, prodynorphin, VGF nerve growth factor inducible) and multiple novel candidate genes possibly involved in cognition (including calcium/calmodulin-dependent protein kinase kinase 2, dual specificity phosphatase 5 and 6, glycophorin C) that were altered following scopolamine treatment. Moreover, we found that stable over-expression of glutamatergic components Homer1a and 1c in the hippocampus of adult rats induced by recombinant adeno-associated virus vector abolished memory improvement produced by the GABA(B) receptor antagonist SGS742 in scopolamine-treated rats. Taken together, these results reveal novel genes and mechanisms involved in scopolamine-induced amnesia, and demonstrate the involvement of both GABA and glutamate neurotransmission in this animal model of cognitive dysfunctions.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Sep
pubmed:issn
0022-3042
pubmed:author
pubmed:issnType
Print
pubmed:volume
102
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
1978-89
pubmed:dateRevised
2011-11-17
pubmed:meshHeading
pubmed-meshheading:17540011-Amnesia, pubmed-meshheading:17540011-Animals, pubmed-meshheading:17540011-Carrier Proteins, pubmed-meshheading:17540011-Disease Models, Animal, pubmed-meshheading:17540011-GABA Antagonists, pubmed-meshheading:17540011-GABA-B Receptor Antagonists, pubmed-meshheading:17540011-Gene Expression Profiling, pubmed-meshheading:17540011-Gene Expression Regulation, pubmed-meshheading:17540011-Genetic Vectors, pubmed-meshheading:17540011-Glutamic Acid, pubmed-meshheading:17540011-Hippocampus, pubmed-meshheading:17540011-Male, pubmed-meshheading:17540011-Muscarinic Antagonists, pubmed-meshheading:17540011-Rats, pubmed-meshheading:17540011-Rats, Long-Evans, pubmed-meshheading:17540011-Receptors, GABA-B, pubmed-meshheading:17540011-Scopolamine Hydrobromide, pubmed-meshheading:17540011-Synaptic Transmission, pubmed-meshheading:17540011-Up-Regulation, pubmed-meshheading:17540011-gamma-Aminobutyric Acid
pubmed:year
2007
pubmed:articleTitle
Hippocampal gene expression profiling reveals the possible involvement of Homer1 and GABA(B) receptors in scopolamine-induced amnesia.
pubmed:affiliation
Department of Neurology & Neurosurgery, Douglas Mental Health University Institute, McGill University, Montréal, Quebec, Canada.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't