The Experts below are selected from a list of 255 Experts worldwide ranked by ideXlab platform

Alain Brunet - One of the best experts on this subject based on the ideXlab platform.

  • epigenetic modulation of Glucocorticoid Receptors in posttraumatic stress disorder
    Translational Psychiatry, 2014
    Co-Authors: Benoit Labonte, N Azoulay, Volodymyr Yerko, Gustavo Turecki, Alain Brunet
    Abstract:

    Some individuals suffering from posttraumatic stress disorder (PTSD) exhibit lower basal salivary cortisol and higher Glucocorticoid receptor (GR) sensitivity. Recent studies suggest that epigenetic mechanisms regulate the activity of cortisol and GR. As a means to combine and cross-validate those findings, we compared cortisol, GR expression and promoter methylation levels in peripheral T lymphocytes of healthy controls versus individuals endorsing a diagnosis of lifetime PTSD. Thirty subjects with lifetime (current or remitted) PTSD and 16 subjects never exposed to trauma were recruited. Salivary cortisol was collected at six time points over the course of a single weekday and analyzed utilizing a time-resolved fluorescence immunoassay. GR expression (GRtotal, 1B, 1C, 1F and 1H) was measured by quantitative RT-PCR. DNA methylation levels in human Glucocorticoid receptor (hGR) 1B and 1C variant's promoter were quantified by epityper in T lymphocytes isolated by magnetic-assisted cell sorting. Individuals with lifetime PTSD have lower morning cortisol release, higher mRNA expression of hGRtotal, 1B, and 1C and lower overall methylation levels in hGR 1B and 1C promoters. Cortisol levels were inversely correlated with hGR 1B mRNA expression. Moreover, overall and CpG site-specific methylation levels were inversely correlated with hGRtotal and 1B mRNA expression. There was no difference between current and remitted PTSD across cortisol, GR expression mRNA and DNA methylation data. Traumatic events induce DNA methylation alterations in distinct promoters of hGR with transcriptional modifications that associate with hypoactive hypothalamus-pituitary-adrenal axis in individuals with PTSD. Our results also point toward an important role of hGR 1B variant in PTSD.

Israel Liberzon - One of the best experts on this subject based on the ideXlab platform.

  • early handling attenuates enhancement of Glucocorticoid Receptors in the prefrontal cortex in an animal model of post traumatic stress disorder
    Biology of mood & anxiety disorders, 2013
    Co-Authors: Sophie A George, Stephanie A Stout, Dayan Knox, Israel Liberzon
    Abstract:

    Background Changes in Glucocorticoid Receptors (GRs) have been implicated in the pathogenesis of stress related psychiatric disorders such as depression and post-traumatic stress disorder (PTSD). Abnormal adaptation of the stress-response system following traumatic stress can lead to an altered hypothalamic-pituitary-adrenal axis that may contribute to PTSD development. Indeed, elevated GR expression in the hippocampus and prefrontal cortex linked to PTSD-like characteristics have been reported in the validated animal model of PTSD, single-prolonged stress. These findings implicate increased levels of GRs in the development of post-traumatic psychopathology and suggest that exploration of GR-targeted interventions may have potential for PTSD prevention. Early handling during the neonatal phase alters GR expression and is proposed to confer resilience to stress. We therefore examined the effects of combined early handling and single prolonged stress treatments on GR expression.

Dayan Knox - One of the best experts on this subject based on the ideXlab platform.

  • early handling attenuates enhancement of Glucocorticoid Receptors in the prefrontal cortex in an animal model of post traumatic stress disorder
    Biology of mood & anxiety disorders, 2013
    Co-Authors: Sophie A George, Stephanie A Stout, Dayan Knox, Israel Liberzon
    Abstract:

    Background Changes in Glucocorticoid Receptors (GRs) have been implicated in the pathogenesis of stress related psychiatric disorders such as depression and post-traumatic stress disorder (PTSD). Abnormal adaptation of the stress-response system following traumatic stress can lead to an altered hypothalamic-pituitary-adrenal axis that may contribute to PTSD development. Indeed, elevated GR expression in the hippocampus and prefrontal cortex linked to PTSD-like characteristics have been reported in the validated animal model of PTSD, single-prolonged stress. These findings implicate increased levels of GRs in the development of post-traumatic psychopathology and suggest that exploration of GR-targeted interventions may have potential for PTSD prevention. Early handling during the neonatal phase alters GR expression and is proposed to confer resilience to stress. We therefore examined the effects of combined early handling and single prolonged stress treatments on GR expression.

Golikov Pp - One of the best experts on this subject based on the ideXlab platform.

  • Effect of morphine derivatives on the function of Glucocorticoid Receptors in shock
    Patologicheskaia fiziologiia i èksperimental'naia terapiia, 1996
    Co-Authors: Golikov Pp, Udovichenko Vi, Kalinin Vn, Kozhevnikova Lm, Marchenko Vv, Moiseev Sk
    Abstract:

    The effects of opiate receptor agonists and antagonists on the function of Glucocorticoid Receptors in the hepatic cytosol were examined in male Wistar rats weighing 180-240 g. With the Scatchard analysis, in vitro experiments by using labelled ligands revealed that the pure opiate agonist morphine in the wide range of concentrations (0,01-10,0 mM) failed to affect the function Type II Glucocorticoid Receptors, though inhibited the function of Type III Glucocorticoid Receptors in the dose-dependent manner. Buprenorphine and diprenorphine depressed the function of Types II and III Glucocorticoid Receptors. Buterphanol, an opiate receptor antagonist-agonist, like naltrexone, an opiate receptor antagonist, decreased the function of Type III Glucocorticoid Receptors, but modulated that of Type II Glucocorticoid Receptors by lowering the association constant of the ligand-Type II Glucocorticoid receptor complex, but by enhancing the density of Type II Glucocorticoid Receptors. In vivo studies established that butorphanol dose-dependently increased the density of Type II Glucocorticoid Receptors in the hepatic cytosol and elevating blood pressure in rat traumatic shock. Whether Glucocorticoid Receptors involve in the mechanism of the antishock effect of morphine derivatives is discussed in the paper.

  • Effect of antibiotics on Glucocorticoid receptor function
    Antibiotics and chemoterapy, 1995
    Co-Authors: Golikov Pp
    Abstract:

    The effects of penicillin G and cefazolin (cefamezin) on the function of the types II and III Glucocorticoid Receptors of the liver cytosol were studied on Wistar male rats weighing 180-200 g. The Scatchard and Lineweaver--Berk analysis showed that penicillin G and cefazolin (0.1-10.0 mM) induced a dose-dependent increase in the density of the type III Glucocorticoid Receptors and a decrease in the affinity of 3H-corticosterone with the type III Glucocorticoid Receptors. The activation of the function of the type III Glucocorticoid receptor by penicillin G and cefazolin was not competitive. Penicillin G had no significant effect on the function of the type II Glucocorticoid Receptors. The increase in the density of the type II Glucocorticoid Receptors under the effect of cefazolin was dose-dependent though Ka and Kd did not significantly change. The results were indicative of the fact that penicillins and cephalosporins had a strong action on the most important regulatory system of homeostasis, i.e. the Glucocorticoid function which is the decisive one in the pathogenesis of inflammation.

  • Modulation of the Glucocorticoid receptor interaction with sodium ethazole
    Voprosy medit︠s︡inskoĭ khimii, 1994
    Co-Authors: Golikov Pp
    Abstract:

    The effect of sodium sulfaethidole on Types II and III Glucocorticoid Receptors was studied in liver cytosol fraction obtained from female Wistar rats of 180-200 g body weight. Functions of Type II Glucocorticoid Receptors in liver cytosol were evaluated by triamcinolone 3H-acetonide and Type III Glucocorticoid Receptors by 3H-corticosterone. The Scatchard and Laynuiver-Berck analyses indicated that sodium sulfaethidole decreased the density of Type II Glucocorticoid Receptors and the complex association constant. A decrease in functions of Type II Glucocorticoid Receptors in the presence of the drug occurred by the competitive type. At the same time, sodium sulfaethidole increased greatly the function of Type III Glucocorticoid Receptors and an increase in the density of these Receptors was realized noncompetitively. The decrease in the functions of Type II Glucocorticoid Receptors and increase in that of Type III Receptors in the presence of sodium sulfaethidole suggest that the drug exhibits antiGlucocorticoid properties.

  • The effect of analgin on Glucocorticoid Receptors
    Eksperimental'naia i klinicheskaia farmakologiia, 1993
    Co-Authors: Golikov Pp
    Abstract:

    Scatchard's analysis was used to examine the specific binding of 3H-acetonide of triamcinolone (3H-AT) by Type II Glucocorticoid Receptors of cytosol from the liver of Wistar rats weighing 180-200 g. It was found that analgin in concentrations of 5.0 and 10.0 mM inhibited the density of Glucocorticoid Receptors and increase the dissociate rate constant of 3H-AT from the receptor and decreased 3H-AT elimination half-life from the receptor. Analgin in concentrations of 0.04, 0.08, 0.16, 0.31, 0.62, 1.25, and 2.50 mM lowered the association constant of the 3H-AT-receptor complex in proportion to the increase of analgin concentrations. Analgin was found to have uncompetitive effects followed by inhibition of the density of Type II Glucocorticoid Receptors.

  • Change in the function of Glucocorticoid Receptors and translocation of Glucocorticoid receptor complexes in hepatocyte nuclei exposed to nonsteroidal drugs
    Patologicheskaia fiziologiia i èksperimental'naia terapiia, 1991
    Co-Authors: Golikov Pp
    Abstract:

    Experiments were conducted on male Wistar rats weighing 180-200 g to study the effect of medical agents (Tizercin 3,5.10(-4) M, 7,0.10(-4) M, Cephazolin, streptomycin and penicillin C--10(-3) M, 10(-4) M) on the function of Glucocorticoid Receptors of hepatic cytosol and translocation of the Glucocorticoid-receptor complexes into the nuclei of hepatocytes. Synthetic labeled ligands 3H-dexamethasone and triamcinolone 3H-acetonide were used. Their specific activity was, respectively, 20 and 22 Ci/mmol The association and dissociation constants and the number of Glucocorticoid-receptor complexes after their translocation into the hepatocyte nuclei were determined by Sketcher's method. It was found that streptomycin and Tizercin inhibit while Cephazolin and penicillin C activate the function of Glucocorticoid Receptors. Translocation of Glucocorticoid-receptor complexes into the hepatocyte nuclei does not change under the effect of these agents.

Sophie A George - One of the best experts on this subject based on the ideXlab platform.

  • early handling attenuates enhancement of Glucocorticoid Receptors in the prefrontal cortex in an animal model of post traumatic stress disorder
    Biology of mood & anxiety disorders, 2013
    Co-Authors: Sophie A George, Stephanie A Stout, Dayan Knox, Israel Liberzon
    Abstract:

    Background Changes in Glucocorticoid Receptors (GRs) have been implicated in the pathogenesis of stress related psychiatric disorders such as depression and post-traumatic stress disorder (PTSD). Abnormal adaptation of the stress-response system following traumatic stress can lead to an altered hypothalamic-pituitary-adrenal axis that may contribute to PTSD development. Indeed, elevated GR expression in the hippocampus and prefrontal cortex linked to PTSD-like characteristics have been reported in the validated animal model of PTSD, single-prolonged stress. These findings implicate increased levels of GRs in the development of post-traumatic psychopathology and suggest that exploration of GR-targeted interventions may have potential for PTSD prevention. Early handling during the neonatal phase alters GR expression and is proposed to confer resilience to stress. We therefore examined the effects of combined early handling and single prolonged stress treatments on GR expression.