The neurotrophin receptors trkA, trkB and trkC are differentially regulated after excitotoxic lesion in rat striatum

Citation
Jm. Canals et al., The neurotrophin receptors trkA, trkB and trkC are differentially regulated after excitotoxic lesion in rat striatum, MOL BRAIN R, 69(2), 1999, pp. 242-248
Citations number
49
Categorie Soggetti
Neurosciences & Behavoir
Journal title
MOLECULAR BRAIN RESEARCH
ISSN journal
0169328X → ACNP
Volume
69
Issue
2
Year of publication
1999
Pages
242 - 248
Database
ISI
SICI code
0169-328X(19990608)69:2<242:TNRTTA>2.0.ZU;2-K
Abstract
In the present work, we examined the time-dependent changes in trkA, trkB a nd trkC mRNA levels induced by the injection of glutamate receptor agonists into the striatum. Changes in trk mRNAs induced by quinolinate, alpha-amin o-3-hydroxy-5-methyl-4-isoxazo-lepropionate (AMPA), kainate or 1S,3R-1-amin ocyclopentane-1,3-dicarboxylic acid (ACPD) were analyzed by a ribonuclease protection assay. All high-affinity neurotrophin receptors showed different ial regulation after intrastriatal injury. Up-regulation of trkA expression was observed in kainate- or ACPD-injected striata at 10 and 24 h, respecti vely, whereas quinolinate injection induced down-regulation between 4 and 6 h after injury. Interestingly, all the excitatory amino acid receptor agon ists induced up-regulation of trkB-kinase mRNA levels. This increase was ma ximal between 2 and 4 h after injection except in kainate injected striata, which showed the peak of expression at 10 h. In contrast, no changes in tr kC mRNA expression were observed after striatal excitotoxic injury. In conc lusion, our results show that trk receptor mRNA levels are differentially r egulated by excitatory amino acid receptor agonists in the striatum, sugges ting that changes in the levels of neurotrophin receptors might be involved either in synaptic plasticity processes or in neuronal protection in the s triatal excitotoxic paradigm. (C) 1999 Elsevier Science B.V. All rights res erved.