DESCRIPTION:

Genes differentially expressed between scopolamine- and saline-treated rats following stimulation in a spatial memory task. Genes down-regulated in scopolamine-treated rats compared to saline-treated animals are indicated by a negative sign whereas genes up-regulated are represented by positive values. Fold changes and bounds of the 95% CI are derived from the average measures obtained with the log2 scale robust multi-array Averaging methods to analyse microarray data.Fold change was uploaded.

LABEL:

Rat drug induced amnesia Genes

SCORE TYPE:

Effect

DATE ADDED:

None

DATE UPDATED:

2024-04-25

SPECIES:

AUTHORS:

Brouillette J, Young D, During MJ, Quirion R

TITLE:

Hippocampal gene expression profiling reveals the possible involvement of Homer1 and GABA(B) receptors in scopolamine-induced amnesia.

JOURNAL:

Journal of neurochemistry Sep 2007, Vol 102, pp. 1978-89

ABSTRACT:

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: 17540011
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