INT13995
From wiki-pain
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Sentences Mentioned In
Key: | Protein | Mutation | Event | Anatomy | Negation | Speculation | Pain term | Disease term |
In both strains, real-time RT-PCR experiments revealed that decreased expression of GR in adolescence and adulthood is, in fact, preceded by increased GR expression during early life stress exposure. | |||||||||||||||
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In contrast to the strain-independent effect of early life stress on GR expression, however, changes in egr-1 expression occurred only in Balb/c mice, and unlike the biphasic developmental changes in GR mRNA expression, egr-1 mRNA was decreased throughout postnatal development. | |||||||||||||||
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However, neither the time of onset nor the mechanism(s) leading to decreased GR expression during postnatal development are known. | |||||||||||||||
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These findings illustrate that the impact of early life stress on gene expression changes is modulated by the genetic background and that the persistent changes in GR and egr-1 expression that arise early during postnatal developmental are reversible by chronic fluoxetine treatment during adolescence and adulthood. | |||||||||||||||
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Thus, in Balb/c mice, changes in GR and egr-1 expression can independently contribute to the phenotypes resulting from early life stress exposure. | |||||||||||||||
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In both strains, real-time RT-PCR experiments revealed that decreased expression of GR in adolescence and adulthood is, in fact, preceded by increased GR expression during early life stress exposure. | |||||||||||||||
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Moreover, there was no consistent overlap of anatomic regions affected by decreased GR and egr-1 protein expression. | |||||||||||||||
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Thus, the early life stress-induced disruption of the normal stress-hyporesponsive period during infancy is accompanied by increased GR expression. | |||||||||||||||
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The present study used two inbred strains of mice that differ in their behavioral responsiveness to stress (Balb/c and C57Bl/6), exposed them to an established paradigm of early life stress (infant maternal separation), and measured their expression of frontal cortical and hippocampal GRs and the putative transcriptional activator of the GR gene, early growth response gene (egr)-1, at defined stages of postnatal development. | |||||||||||||||
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Glucocorticoid receptor-impaired (GR-i) mice, a transgenic model for affective disorders with hypothalamic-pituitary-adrenal (HPA) axis feedback control deficit, were used to assess the antidepressant-like effects of the mixed melatonin receptor agonist/5-HT(2C) receptor antagonist, agomelatine, compared to the selective 5-HT reuptake inhibitor (SSRI), fluoxetine, on hippocampal neurogenesis, GR and BDNF expression and antidepressant-responsive behaviour (tail suspension test, TST). | |||||||||||||||
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Fluoxetine decreased glucocorticoid receptor (GR) gene expression in the prefrontal cortex, amygdala, locus coeruleus and dorsal raphé nucleus, and increased locus coeruleus tyrosine hydroxylase and dorsal raphé nucleus tryptophan hydroxylase-2 (TPH2) gene expression. | |||||||||||||||
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The GR was present in neuronal populations with classical neurotransmitters, especially monoamines and glutamate and with various neuropeptides. | |||||||||||||||
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The GR is found already in the fetal rat and the development of GR mRNA and receptor protein was followed during the pre- and postnatal periods. | |||||||||||||||
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The beneficial effect of CpdA required expression of the GR in T cells and was achieved by down regulating LFA-1 and CD44 on peripheral Th cells and by repressing IL-17 production.
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Corticosterone readily passes the bloodbrain barrier and the GR is highly expressed throughout the motive circuit and the limbic system (Reul and De Kloet 1985; Fuxe et al. 1985; Harfstrand et al. 1986). | |||||||||||||||
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Therefore, GR-mediated gene expression in the striatum may play a role in the chronic effects of morphine and could be involved in the formation of drug-associated behavior. | |||||||||||||||
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Since it is believed that beneficial effects are often mediated by GR transrepression while many side effects rely on GR transactivation, current research aims at identifying novel substances that dissociate these two features. | |||||||||||||||
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Flow cytometric analysis confirmed our earlier findings in thymocytes showing that GR inactivation compromised Dex-induced cell death in WEHI 7.1 cells while the pro-apoptotic activity of CpdA was unaffected (Fig. 3C,D). | |||||||||||||||
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5 M CpdA did not alter the expression of the bona fide GR target gene glucocorticoid-induced leucin zipper (GILZ) in Tenc cells while treatment with 10? | |||||||||||||||
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Therefore we studied GR expression, as well as the serum cortisol levels, in patients with recently diagnosed RA. | |||||||||||||||
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