Neuroscience 2005 Abstract
| Presentation Number: | 448.5 |
|---|---|
| Abstract Title: | Gene expression in an animal model of autism using DNA microarrays and real time-PCR. |
| Authors: |
Toledo-Rodriguez, M.*1
; Antoniello, K.1
; Rinaldi, T.1
; Markram, H.1
1Brain Mind Inst., Ecole Polytechinque Federale de Lausanne (EPFL), lausanne, Switzerland |
| Primary Theme and Topics |
Disorders of the Nervous System - Cognitive, Emotional and Behavioral State Disorders -- Autism, mental retardation, and related disorders |
| Session: |
448. Autism: Animal Models and Clinical Studies Poster |
| Presentation Time: | Monday, November 14, 2005 8:00 AM-9:00 AM |
| Location: | Washington Convention Center - Hall A-C, Board # UU44 |
| Keywords: | ION CHANNEL, GLUTAMATE RECEPTOR, disease, NEOCORTEX |
Autism is a complex neurodevelopmental disorder, characterized by impaired social and executive function, repetitive and stereotyped behaviors and focused interests. Autism has a strong genetic predisposition since there is more than 50% concordance among monozygotic twins while the normal incidence is around 0.2% (Folstein and Rosen-Seidley 2001). A number of genes have been implicated in autism including AMPA, canabinoid and somatostatin receptors (Purcell et al. Neurolog 2001). In an electrophysiological study (Rinaldi, SFN 2005 Abstract), we found that the microcircuit is hyper-connected with hypoexcitable pyramidal neurons in an animal model of autism – prenatal exposure to valproic acid (VPA, Ingram et al. NeuroToxicol Teratol 2000). Reverse predictions implicate the expression of Kv2.2, Kv3.3, SK2 and Ca1A ion channels in the hypoexcitability. We studied the changes in gene expression at the single cell level in this model for autism using oligonucleotide microarrays and real time PCR. For this purpose single pyramidal cells in layer 5 were harvested using Laser Capture Microscopy (LCM) in Primary Somatosensory Cortex and Prefrontal Cortex in control and VPA treated Wistar rats. Between 500-1000 cells from each condition (layer-cortical area-treatment) were pooled, their RNA was extracted and amplified. The amplified RNA was used to either label oligonucleotide microarrays or perform real time PCR for genes suspected to be differentially expressed in this model of autism. Subsequently the differential gene expression between treated and control animals were analyzed and the differentially expressed genes were confirmed by real time PCR and/or immunohistochemistry.α.
Sample Citation:
[Authors]. [Abstract Title]. Program No. XXX.XX. 2005 Neuroscience Meeting Planner. Washington, DC: Society for Neuroscience, 2005. Online.
Copyright © 2005-2026 Society for Neuroscience; all rights reserved. Permission to republish any abstract or part of any abstract in any form must be obtained in writing by SfN office prior to publication.
