Cognitive dysfunction in NF1 knock-out mice may result from altered vesicular trafficking of APP/DRD3 complex

BMC Neuroscience
Elizabeth A DonarumVinodh Narayanan

Abstract

It has been estimated that more than 50% of patients with Neurofibromatosis type 1 (NF1) have neurobehavioral impairments which include attention deficit/hyperactivity disorder, visual/spatial learning disabilities, and a myriad of other cognitive developmental problems. The biological mechanisms by which NF1 gene mutations lead to such cognitive deficits are not well understood, although excessive Ras signaling and increased GABA mediated inhibition have been implicated. It is proposed that the cognitive deficits in NF1 are the result of dysfunctional cellular trafficking and localization of molecules downstream of the primary gene defect. To elucidate genes involved in the pathogenic process, gene expression analysis was performed comparing the expression profiles in various brain regions for control and Nf1+/- heterozygous mice. Gene expression analysis was performed for hippocampal samples dissected from postnatal day 10, 15, and 20 mice utilizing the Affymetrix Mouse Genome chip (Murine 430 2.0). Analysis of expression profiles between Nf1+/- and wild-type animals was focused on the hippocampus because of previous studies demonstrating alterations in hippocampal LTP in the Nf1+/- mice, and the region's importance in visual...Continue Reading

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Citations

Jun 25, 2013·European Neuropsychopharmacology : the Journal of the European College of Neuropsychopharmacology·Shinichiro NakajimaAriel Graff-Guerrero
Oct 28, 2011·Neuropsychopharmacology : Official Publication of the American College of Neuropsychopharmacology·David J G WatsonKevin C F Fone
Oct 31, 2020·Cells·Mohammed BergougHélène Bénédetti

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Methods Mentioned

BETA
GTPase
targeted mutations
gene knock-out
genetic modification
PCR
electrophoresis
chip
in vitro transcription

Software Mentioned

Array Data Manipulation
GeneSpring
GeneGo
Affymetrix Microarray Suite

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