Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:3.1.27.5 (RNase)
 17,967 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In the present work, we examined the time-dependent changes in trkA, trkB and trkC mRNA levels induced by the injection of glutamate receptor agonists into the striatum. Changes in trk mRNAs induced by quinolinate, alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionate (AMPA), kainate or 1S,3R-1-aminocyclopentane-1,3-dicarboxylic acid (ACPD) were analyzed by a ribonuclease protection assay. All high-affinity neurotrophin receptors showed differential regulation after intrastriatal injury. Up-regulation of trkA expression was observed in kainate- or ACPD-injected striata at 10 and 24 h, respectively, whereas quinolinate injection induced down-regulation between 4 and 6 h after injury. Interestingly, all the excitatory amino acid receptor agonists induced up-regulation of trkB-kinase mRNA levels. This increase was maximal 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 trkC mRNA expression were observed after striatal excitotoxic injury. In conclusion, our results show that trk receptor mRNA levels are differentially regulated by excitatory amino acid receptor agonists in the striatum, suggesting that changes in the levels of neurotrophin receptors might be involved either in synaptic plasticity processes or in neuronal protection in the striatal excitotoxic paradigm.
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PMID:The neurotrophin receptors trkA, trkB and trkC are differentially regulated after excitotoxic lesion in rat striatum. 1036 45

Infection of newborn rats with Borna disease virus (BDV) leads to persistence in the absence of overt signs of inflammation. BDV persistence, however, causes cerebellar hypoplasia and hippocampal dentate gyrus neuronal cell loss, which are accompanied by diverse neurobehavioral abnormalities. Neurotrophins and their receptors play important roles in the differentiation and survival of hippocampal and cerebellar neurons. We have examined whether BDV can cause alterations in the neurotrophin network, thus promoting neuronal damage. We have used RNase protection assay to measure mRNA levels of the neurotrophins nerve growth factor (NGF), brain-derived neurotrophic factor (BDNF), and neurotrophin-3 (NT-3), and their trkC and trkB receptors, as well as the growth factors insulin-like growth factor I (IGF-1) and basic fibroblast growth factor (bFGF), in the cerebellum and hippocampus of BDV-infected and control rats at different time points p.i. Reduced mRNA expression levels of NT-3, BDNF and NGF were found after day 14 p.i. in the hippocampus, but not in the cerebellum, of newborn infected rats. Three weeks after infection, trkC mRNA expression levels were reduced in both hippocampus and cerebellum of infected rats, whereas decreased trkB mRNA levels were only observed in the cerebellum. Reduced trkC mRNA expression was confined to the dentate gyrus of the hippocampus, as assessed by in situ hybridization. TUNEL assay revealed massive apoptotic cell death in the dentate gyrus of infected rats at days 27 and 33 p.i. Increased numbers of apoptotic cells were also detected in the cerebellar granular layer of infected rats after 8 days p.i. Moreover, a dramatic loss of cerebellar Purkinje cells was seen after day 27 p.i. Our results support the hypothesis, that BDV-induced alterations in neurotrophin systems might contribute to selective neuronal cell death.
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PMID:Alterations in neurotrophin and neurotrophin receptor gene expression patterns in the rat central nervous system following perinatal Borna disease virus infection. 1117 19

During development neurons are protected against various insults by intrinsic properties. Here we evaluate trkB (both full-length and truncated forms) and trkC expression in the striatum, cortex, and substantia nigra after intrastriatal injection of quinolinic acid (QUIN) at different stages of postnatal (P) development, by RNase protection assay and in situ hybridization. During normal development, a region-specific regulation of trkB and trkC was observed, showing the maximal mRNA levels at P5. Excitotoxic lesion did not modify striatal trkB mRNA levels at any age examined. However, trkC decreased after QUIN injection at P5 in the striatum (52 +/- 2% of control levels). On the other hand, regulation of trkB and trkC expression was observed in cortex and substantia nigra after striatal excitotoxic lesion. Both full-length and truncated receptor isoforms of trkB were enhanced in the cortex when striatal injury was produced at P21 (268 +/- 38 and 206 +/- 35%) or P30 (174 +/- 35 and 157 +/- 13%). In situ hybridization studies localized this increase in trkB expression in layers II/III and V along the cerebral cortex. Within the substantia nigra, striatal excitotoxicity at P5 selectively decreased the truncated form of trkB (70 +/- 7%), whereas the full-length form was up-regulated at P30 (130 +/- 2%). A biphasic increase in trkC mRNA levels was observed at P5 (151 +/- 3%) and P21 (168 +/- 4%). These changes were localized in the substantia nigra pars compacta. Triple-labeling studies disclosed that all these changes were mainly located in neurons. These results demonstrate that the endogenous response to excitotoxicity includes transneuronal regulation of neurotrophin receptors, which is specific for each nucleus and depends on the developmental stage.
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PMID:TrkB and TrkC are differentially regulated by excitotoxicity during development of the basal ganglia. 1171 53


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