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Microarray analysis of gene expression in the rat vestibular nucleus complex following unilateral vestibular deafferentation
Author(s) -
Horii Arata,
Masumura Chisako,
Smith Paul F.,
Darlington Cynthia L.,
Kitahara Tadashi,
Uno Atsuhiko,
Mitani Kenji,
Kubo Takeshi
Publication year - 2004
Publication title -
journal of neurochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.75
H-Index - 229
eISSN - 1471-4159
pISSN - 0022-3042
DOI - 10.1111/j.1471-4159.2004.02781.x
Subject(s) - biology , gene , protein subunit , vestibular system , microbiology and biotechnology , gene expression , vestibular nuclei , neuroscience , genetics
Abstract To investigate the molecular background of vestibular compensation, a model of lesion‐induced plasticity, we used a microarray analysis to examine genes that show asymmetrical expression between the bilateral vestibular nucleus complexes (VNCs) 6 h following unilateral vestibular deafferentation (UVD). Asymmetrical gene expression was then validated by a real‐time quantitative PCR. Among the 88 genes for which the ipsilateral (ipsi) : contralateral (contra) was > 1.35, the number of known genes was 33 (38%), and the number of expressed sequence tag (EST) sequences was 55 (62%). Among the 130 genes for which the contra : ipsi was > 1.35, the number of known genes was 55 (42%), and the number of EST sequences was 75 (58%). Changes in some of the genes were consistent with previous studies; however, we found several new genes which could be functionally related to the molecular basis of the electrophysiological asymmetry between the VNCs following UVD. Ipsi > contra genes included the GABA A receptor rho subunit, regulatory proteins of G protein signaling, calcium signaling related molecules such as the voltage‐dependent calcium channel α2/δ subunit 1, calcineurin subunit Aβ and Ca 2+ pump. Contra > ipsi genes included the neuronal high affinity glutamate transporter, 5‐hydroxytryptamine receptor 1D, mitogen‐activated protein kinase 12 and ubiquitin carboxy‐terminal hydrolase L1.