Psychophysiological stress‐regulated gene expression in mice

Murata, Shigenori; Yoshiara, Taeko; Lim, Chun Ren; Sugino, Maiko; Kogure, Mitori; Ohnuki, Tatsuya; Komurasaki, Toshi; Matsubara, Kazuo

doi:10.1016/j.febslet.2005.02.069

Cited by 27 publications

(18 citation statements)

References 31 publications

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“…This gene was at the top of the list of genes regulated, both, by dexamethasone in cultured astrocytes and by morphine in the mouse striatum. Alterations in the level of Sgk1 transcript or protein have been previously observed in the CNS in various models of stress (Koya et al, 2005;Murata et al, 2005;Yuen et al, 2010), after exposure to dexamethasone (Sato et al, 2008;David et al, 2005;van Gemert et al, 2006), drugs of abuse (Piechota et al, 2010b) and antidepressants (Conti et al, 2007), as well as in animal models of memory formation (von Hertzen and Giese, 2005) and neurodegeneration (Iwata et al, 2004;Rangone et al, 2004;Schoenebeck et al, 2005). Our results show that GR-responsive isoforms of Sgk1 are confined to astrocytes.…”

Section: Regulation Of Sgk1 Expression In Neural Cellssupporting

confidence: 73%

Astrocytes are a neural target of morphine action via glucocorticoid receptor‐dependent signaling

Ślęzak

Korostyński

Gieryk

et al. 2013

Glia

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Chronic opioid use leads to the structural reorganization of neuronal networks, involving genetic reprogramming in neurons and glial cells. Our previous in vivo studies have revealed that a significant fraction of the morphine-induced alterations to the striatal transcriptome included glucocorticoid (GC) receptor (GR)-dependent genes. Additional analyses suggested glial cells to be the locus of these changes. In the current study, we aimed to differentiate the direct transcriptional effects of morphine and a GR agonist on primary striatal neurons and astrocytes. Whole-genome transcriptional profiling revealed that while morphine had no significant effect on gene expression in both cell types, dexamethasone significantly altered the transcriptional profile in astrocytes but not neurons. We obtained a complete dataset of genes undergoing the regulation, which includes genes related to glucose metabolism (Pdk4), circadian activity (Per1) and cell differentiation (Sox2). There was also an overlap between morphine-induced transcripts in striatum and GR-dependent transcripts in cultured astrocytes. We further analyzed the regulation of expression of one gene belonging to both groups, serum and GC regulated kinase 1 (Sgk1). We identified two transcriptional variants of Sgk1 that displayed selective GR-dependent upregulation in cultured astrocytes but not neurons. Moreover, these variants were the only two that were found to be upregulated in vivo by morphine in a GR-dependent fashion. Our data suggest that the morphine-induced, GR-dependent component of transcriptome alterations in the striatum is confined to astrocytes. Identification of this mechanism opens new directions for research on the role of astrocytes in the central effects of opioids. V V C 2013 Wiley Periodicals, Inc.

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Section: Regulation Of Sgk1 Expression In Neural Cellssupporting

confidence: 73%

Astrocytes are a neural target of morphine action via glucocorticoid receptor‐dependent signaling

Ślęzak

Korostyński

Gieryk

et al. 2013

Glia

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“…We demonstrate that Sgk1 expression is regulated similarly in males and females, and is insensitive to the effects of handling. Previous work has demonstrated that even after a prolonged period of severe stress -6 hrs of restraint water submersion -a similar two-fold increase in Sgk1 mRNA levels could be detected (Murata et al, 2005), suggesting that a sufficiently strong stressor can cause rapid and persistent activation of Sgk1 in the hippocampus. Our finding that stress-induced Sgk1 induction is independent of corticosterone and Crhr1 is in contrast with in vitro studies that report increased Sgk1 expression by corticosterone in cultured hippocampal progenitor cells (Anacker et al, 2013), as well as by Crh via Crhr1 signaling (Sheng et al, 2008).…”

Section: Discussionmentioning

confidence: 87%

Hippocampal gene expression induced by cold swim stress depends on sex and handling

Bohacek

Manuella

Roszkowski

et al. 2015

Psychoneuroendocrinology

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Summary: Stress-related disorders such as PTSD and depression are more prevalent in women than men. One reason for such discordance may be that brain regions involved in stress responses are more sensitive to stress in females. Here, we compared the effects of acute stress on gene transcription in the hippocampus of female and male mice, and also examined the involvement of two key stress-related hormones, corticosterone and corticotropin releasing hormone (Crh). Using quantitative reverse transcription polymerase chain reaction (RT-qPCR), we measured gene expression of Fos, Per1 and Sgk1 45 min after exposure to brief cold swim stress. Stress induced a stronger increase in Fos and Per1 expression in females than males. The handling control procedure increased Fos in both sexes, but occluded the effects of stress in males. Further, handling increased Per1 only in males. Sgk1 was insensitive to handling, and increased in response to stress similarly in males and females. The transcriptional changes observed after swim stress were not mimicked by corticosterone injections, and the stress-induced increase in Fos, Per1 and Sgk1 could neither be prevented by pharmacologically blocking glucocorticoid receptor (GR) nor by blocking Crh receptor 1 (Crhr1) before stress exposure. Finally, we demonstrate that the effects are stressor-specific, as the expression of target genes could not be increased by brief restraint stress in either sex. In summary, we find strong effects of acute swim stress on hippocampal gene expression, complex interactions between handling and sex, and a remarkably unique response pattern for each gene. Overall, females respond to a cold swim challenge with stronger hippocampal gene transcription than males, independent of two classic mediators of the stress response, corticosterone and Crh. These findings may have important implications for understanding the higher vulnerability of women to certain stress-related neuropsychiatric diseases. In summary, we find strong effects of acute swim stress on hippocampal gene expression, complex interactions between handling and sex, and a remarkably unique response pattern for each gene. Overall, females respond to a cold swim challenge with stronger hippocampal gene transcription than males, independent of two classic mediators of the stress response, corticosterone and Crh. These findings may have important implications for understanding the higher vulnerability of women to certain stress-related neuropsychiatric diseases.

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“…Thus, for the functional validation of some transcripts identified as possible drug targets, further studies will be necessary to assess the effect of transcriptional regulation in one or more rodent models of depression. [38][39][40][41][42][43] Another apparent limitation is that transcriptional profiles for the different treatments were compared only at the time points corresponding to clinical efficacy, which differed for each treatment being 2 days for ECT, 1 day for SD and 14 days for FLX. Thus, a comparative analysis of transcriptional changes induced at the same time points for all treatments is missing.…”

Section: Number Of Transcripts Affected By Single and Multiple Treatmmentioning

confidence: 99%

“…98 Sgk1 expression level is increased by acute amphetamine 36 and lysergic acid diethylamide (LSD) treatment, 36 and it is increased in the brain and peripheral tissues following psychosocial stress. 40 The upregulation of Sgk1 strongly correlates with the occurrence of cell death. In Mecp2-null mice, a model for Rett syndrome, 99 increased levels of Sgk1 mRNA are reported before and after onset of neurological symptoms.…”

Section: Number Of Transcripts Affected By Single and Multiple Treatmmentioning

confidence: 99%

Region-specific transcriptional changes following the three antidepressant treatments electro convulsive therapy, sleep deprivation and fluoxetine

et al. 2006

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The significant proportion of depressed patients that are resistant to monoaminergic drug therapy and the slow onset of therapeutic effects of the selective serotonin reuptake inhibitors (SSRIs)/serotonin/noradrenaline reuptake inhibitors (SNRIs) are two major reasons for the sustained search for new antidepressants. In an attempt to identify common underlying mechanisms for fast-and slow-acting antidepressant modalities, we have examined the transcriptional changes in seven different brain regions of the rat brain induced by three clinically effective antidepressant treatments: electro convulsive therapy (ECT), sleep deprivation (SD), and fluoxetine (FLX), the most commonly used slow-onset antidepressant. Each of these antidepressant treatments was applied with the same regimen known to have clinical efficacy: 2 days of ECT (four sessions per day), 24 h of SD, and 14 days of daily treatment of FLX, respectively. Transcriptional changes were evaluated on RNA extracted from seven different brain regions using the Affymetrix rat genome microarray 230 2.0. The gene chip data were validated using in situ hybridization or autoradiography for selected genes. The major findings of the study are:1. The transcriptional changes induced by SD, ECT and SSRI display a regionally specific distribution distinct to each treatment. 2. The fast-onset, short-lived antidepressant treatments ECT and SD evoked transcriptional changes primarily in the catecholaminergic system, whereas the slow-onset antidepressant FLX treatment evoked transcriptional changes in the serotonergic system. 3. ECT and SD affect in a similar manner the same brain regions, primarily the locus coeruleus, whereas the effects of FLX were primarily in the dorsal raphe and hypothalamus, suggesting that both different regions and pathways account for fast onset but short lasting effects as compared to slow-onset but long-lasting effects. However, the similarity between effects of ECT and SD is somewhat confounded by the fact that the two treatments appear to regulate a number of transcripts in an opposite manner. 4. Multiple transcripts (e.g. brain-derived neurotrophic factor (BDNF), serum/glucocorticoidregulated kinase (Sgk1)), whose level was reported to be affected by antidepressants or behavioral manipulations, were also found to be regulated by the treatments used in the present study. Several novel findings of transcriptional regulation upon one, two or all three treatments were made, for the latter we highlight homer, erg2, HSP27, the proto oncogene ret, sulfotransferase family 1A (Sult1a1), glycerol 3-phosphate dehydrogenase (GPD3), the orphan receptor G protein-coupled receptor 88 (GPR88) and a large number of expressed sequence tags (ESTs). 5. Transcripts encoding proteins involved in synaptic plasticity in the hippocampus were strongly affected by ECT and SD, but not by FLX.The novel transcripts, concomitantly regulated by several antidepressant treatments, may represent novel targets for fast onset, long-duration antidepressants.

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Psychophysiological stress‐regulated gene expression in mice

Cited by 27 publications

References 31 publications

Astrocytes are a neural target of morphine action via glucocorticoid receptor‐dependent signaling

Astrocytes are a neural target of morphine action via glucocorticoid receptor‐dependent signaling

Hippocampal gene expression induced by cold swim stress depends on sex and handling

Region-specific transcriptional changes following the three antidepressant treatments electro convulsive therapy, sleep deprivation and fluoxetine

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