Differential stress response in rats subjected to chronic mild stress is accompanied by changes in CRH-family gene expression at the pituitary level

Kolasa, Magdalena; Faron-Górecka, Agata; Kuśmider, Maciej; Szafran-Pilch, Kinga; Solich, Joanna; Żurawek, Dariusz; Gruca, Piotr; Papp, Mariusz; Dziedzicka-Wasylewska, Marta

doi:10.1016/j.peptides.2014.09.008

Cited by 14 publications

(24 citation statements)

References 65 publications

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“…In this model, rats were subjected to 2 weeks of daily stress and behaviorally characterized using the sucrose consumption test into differently reacting groups based on their response to stress, i.e., anhedonic (stress-reactive, stress-R), stress-resilient (stress-non-reactive, stress-NR), and invert reactive rats (characterized by excessive sucrose intake, stress-IR). The occurrence of resistance (or rather resilience) or susceptibility to stress in animals subjected to CMS has recently gained the interest of researchers (Bergström et al 2008 ; Taliaz et al 2011 ; Delgado y Palacios et al 2011 ; Christensen et al 2011 ; Żurawek et al 2013 ; Faron-Górecka et al 2014 ; Kolasa et al 2014 ; Czéh et al 2015 ), but the molecular signature underlying the observed differences in the behavioral responses to stress still remains unresolved. Since the previously obtained data suggested the role of SST in stress and depression, we decided to measure specific binding of [ 125 I]Tyr 3 -Octreotide.…”

Section: Introductionmentioning

confidence: 99%

Chronic mild stress alters the somatostatin receptors in the rat brain

et al. 2015

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RationaleThe involvement of somatostatin (SST) and its receptors in the pathophysiology of depression and stress has been evidenced by numerous studies.ObjectivesThe purpose of the present study was to find whether chronic mild stress (CMS), an animal model of depression, affects the SST receptors in the rat brain and pituitary, as well as the level of SST in plasma.MethodsIn CMS model, rats were subjected to 2 weeks of stress and behaviorally characterized using the sucrose consumption test into differently reacting groups based on their response to stress, i.e., stress-reactive (anhedonic), stress-non-reactive (resilient), and invert-reactive rats (characterized by excessive sucrose intake). We measured specific binding of [125I]Tyr3-Octreotide, expression of mRNA encoding sst2R receptors in the rat brains, expression of SST and its receptors in rat pituitary, and the level of SST in the plasma.ResultsThe obtained results show decreases in binding of [125I]Tyr3-Octreotide in most of rat brain regions upon CMS and no significant differences between three stressed groups of animals, except for significant up-regulation of sst2 receptor in medial habenula (MHb) in the stress-reactive group. In the same group of animals, significant increase in plasma SST level was observed.ConclusionsThere are two particularly sensitive sites distinguishing the response to stress in CMS model. In the brain, it is MHb, while on the periphery this predictor is SST level in plasma. These changes may broaden an understanding of the mechanisms involved in the stress response and point to the intriguing role of MHb.

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Section: Introductionmentioning

confidence: 99%

Chronic mild stress alters the somatostatin receptors in the rat brain

et al. 2015

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“…Walker et al 2015) or a more sensitive assay of HPA axis activity (e.g. serum ACTH levels or ACTH/corticosterone ratio, or measures of pituitary gene expression; Kolasa et al 2014) may be required to reveal an effect of pharmacologically activated RXFP3 signalling on elements of the mouse HPA axis.…”

Section: Discussionmentioning

confidence: 99%

Relaxin-3/RXFP3 signalling in mouse hypothalamus: no effect of RXFP3 activation on corticosterone, despite reduced presynaptic excitatory input onto paraventricular CRH neurons in vitro

et al. 2017

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Relaxin-3/RXFP3 signalling is proposed to be involved in the neuromodulatory control of arousal- and stress-related neural circuits. Furthermore, previous studies in rats have led to the proposal that relaxin-3/RXFP3 signalling is associated with activation of the hypothalamic-pituitary-adrenal axis, but direct evidence for RXFP3-related actions on the activity of hypothalamic corticotropin-releasing hormone (CRH) neurons is lacking. In this study, we investigated characteristics of the relaxin-3/RXFP3 system in mouse hypothalamus. Administration of an RXFP3 agonist (RXFP3-A2) intra-cerebroventricularly or directly into the paraventricular nucleus of hypothalamus (PVN) of C57BL/6J mice did not alter corticosterone levels. Similarly, there were no differences between serum corticosterone levels in Rxfp3 knockout (C57BL/6J) and wild-type mice at baseline and after stress, despite detection of the predicted stress-induced increases in serum corticosterone. We examined the nature of the relaxin-3 innervation of PVN in wild-type mice and in Crh-IRES-Cre;Ai14 mice that co-express the tdTomato fluorophore in CRH neurons, identifying abundant relaxin-3 fibres in the peri-PVN region, but only sparse fibres associated with densely packed CRH neurons. In whole-cell voltage-clamp recordings of tdTomato-positive CRH neurons in these mice, we observed a reduction in sEPSC frequency following local application of RXFP3-A2, consistent with an activation of RXFP3 on presynaptic glutamatergic afferents in the PVN region. These studies clarify the relationship between relaxin-3/RXFP3 inputs and CRH neurons in mouse PVN, with implications for the interpretation of current and previous in vivo studies and future investigations of this stress-related signalling network in normal and transgenic mice, under normal and pathological conditions.

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“…It is difficult to explain why the increase in the concentrations of G-6-P and glycogen or expression of mitochondrial complex V was more visible in the frontal cortex in stress-nonreactive than stressreactive animals. It is known, that not all animals respond to some stress procedures used in animal models of depression with behavioral depression-like symptoms, but they predominantly cause similar biochemical changes (Kolasa et al 2014;Kurek et al 2018). Maybe some of these changes are adaptive and delay the onset of pro-depressive behavior.…”

Section: Frontal Cortex Hippocampusmentioning

confidence: 99%

“…Additionally, since prenatal stress was used in the present study as an animal model of depression and not all animals evoked depression-like behavioral changes, (which were verified by an increase in immobility time in the Porsolt test), prenatally stressed rats were divided into prenatal stress-reactive (PS-R) and prenatal stress-nonreactive (PS-NR) groups. Despite the use of identical stressors, not all animals show depression-like behavior; such a situation has also been observed in other animal models of this disease (Kolasa et al 2014). Selected metabolic markers were determined in the hippocampus and frontal cortex, since changes are mainly observed in those structures in depression and the adverse effects of prenatal stress occur in these structures as well.…”

Section: Introductionmentioning

confidence: 97%

Brain Metabolic Alterations in Rats Showing Depression-Like and Obesity Phenotypes

et al. 2019

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Current data suggest an important role of brain metabolic disturbances in the pathogenesis of depression and obesity, diseases that frequently co-occur. Our aim was to determine whether there are changes in markers characterizing glucose metabolism in prenatal stress (PS; animal model of depression), in rats fed a high-fat diet (HFD), and especially in the model of depression and obesity co-occurrence. The changes in glucose-6-phosphate, glycogen, glucose transporters (GLUT1, GLUT4), glucagonlike peptide-1 receptor (GLP-1R), and mitochondrial complexes levels in the frontal cortex and/or hippocampus were observed. In the case of the coexistence of depression and obesity, the most important changes were (1) the decrease in the membrane form of GLUT4, which may suggest weaker insulin action in the frontal cortex, and (2) the diminished GLP-1R, which could cause neurodegenerative changes in the hippocampus. However, presented results suggested that HFD weakened the PS effect of uncoupling oxidative phosphorylation in the frontal cortex.

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Differential stress response in rats subjected to chronic mild stress is accompanied by changes in CRH-family gene expression at the pituitary level

Cited by 14 publications

References 65 publications

Chronic mild stress alters the somatostatin receptors in the rat brain

Chronic mild stress alters the somatostatin receptors in the rat brain

Relaxin-3/RXFP3 signalling in mouse hypothalamus: no effect of RXFP3 activation on corticosterone, despite reduced presynaptic excitatory input onto paraventricular CRH neurons in vitro

Brain Metabolic Alterations in Rats Showing Depression-Like and Obesity Phenotypes

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