Differential expression of Dusp1 and immediate early response genes in hippocampus of rats, subjected to forced swimming test
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ABSTRACT:
ORGANISM(S): Rattus norvegicus
PROVIDER: GSE162524 | GEO | 2023/02/27
REPOSITORIES: GEO
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Project description:The circadian clock system is associated with feeding and mood. Patients with night eating syndrome (NES) delay their eating rhythm and their mood declines during the evening and night, manifesting as time-specific depression. Therefore, we hypothesized that the NES feeding pattern might cause time-specific depression. We established new NES model by restricted feeding with high-fat diet during the inactive period under normal-fat diet ad libitum. The FST (forced swimming test) immobility time in the NES model group was prolonged only after lights-on, corresponding to evening and early night for humans. We examined the effect of the NES feeding pattern on peripheral clocks using PER2::LUCIFERASE knock-in mice and an in vivo monitoring system. Caloric intake during the inactive period would shift the peripheral clock, and might be an important factor in causing the time-specific depression-like behavior. In the NES model group, synthesis of serotonin and norepinephrine were increased, but utilization and metabolism of these monoamines were decreased under stress. Desipramine shortened some mice's FST immobility time in the NES model group. The present study suggests that the NES feeding pattern causes phase shift of peripheral clocks and malfunction of the monoamine system, which may contribute to the development of time-specific depression.
| S-EPMC5773531 | biostudies-other
Project description:BackgroundMany neuropsychiatric disorders, including stress-related mood disorders, are complex multi-parametric syndromes. Susceptibility to stress and depression is individually different. The best animal model of individual differences that can be used to study the neurobiology of affect regards spontaneous reactions to novelty. Experimentally, when naive rats are exposed to the stress of a novel environment, they display a highly variable exploratory activity and are classified as high or low responders (HR or LR, respectively). Importantly, HR and LR rats do not seem to exhibit a substantial differentiation in relation to their 'depressive-like' status in the forced swim test (FST), a widely used animal model of 'behavioral despair'. In the present study, we investigated whether FST exposure would be accompanied by phenotype-dependent differences in hippocampal gene expression in HR and LR rats.ResultsHR and LR rats present a distinct behavioral pattern in the pre-test session but develop comparable depressive-like status in the second FST session. At 24 h following the second FST session, HR and LR rats (stressed and unstressed controls) were sacrificed and hippocampal samples were independently analyzed on whole rat genome Illumina arrays. Functional analysis into pathways and networks was performed using Ingenuity Pathway Analysis (IPA) software. Notably, hippocampal gene expression signatures between HR and LR rats were markedly divergent, despite their comparable depressive-like status in the FST. These molecular differences are reflected in both the extent of transcriptional remodeling (number of significantly changed genes) and the types of molecular pathways affected following FST exposure. A markedly higher number of genes (i.e., 2.28-fold) were statistically significantly changed following FST in LR rats, as compared to their HR counterparts. Notably, genes associated with neurogenesis and synaptic plasticity were induced in the hippocampus of LR rats in response to FST, whereas in HR rats, FST induced pathways directly or indirectly associated with induction of apoptotic mechanisms.ConclusionsThe markedly divergent gene expression signatures exposed herein support the notion that the hippocampus of HR and LR rats undergoes distinct transcriptional remodeling in response to the same stress regimen, thus yielding a different FST-related 'endophenotype', despite the seemingly similar depressive-like phenotype.
| S-EPMC3941591 | biostudies-literature
Project description:PurposeWe developed a method for quantifying intraoperative torsional forced ductions and validated the new test by comparing patients with oblique dysfunction and controls.DesignComparative case series.SubjectsWe studied 33 eyes with oblique dysfunction (9 with presumed congenital superior oblique palsy [SOP], 13 with acquired SOP, 7 with Brown syndrome, and 4 with inverted Brown syndrome) and 31 controls. We also studied 6 eyes after superior oblique (SO) disinsertion and 2 eyes after inferior oblique (IO) disinsertion.MethodsUnder deep general anesthesia, the 12 and 6 o'clock positions at the limbus were marked and the globe was maximally excyclorotated and incyclorotated without retroplacement until the first resistance was felt, and the angle of rotation (in degrees) was read on a Mendez ring by the surgeon. A photograph was taken in each position to be read by a masked observer.Main outcome measuresMaximal excyclorotation and maximal incyclorotation in each oblique dysfunction and in controls by both surgeon's report and photographic assessment. We duplicated the photographs to evaluate test-retest reliability and to evaluate agreement between the surgeon's assessments and the photographic assessment.ResultsSurgeon's assessment revealed greater maximal excyclorotation in eyes with presumed congenital SOP than in controls (median, 40 vs. 30 degrees). Maximal excyclorotation in eyes with acquired SOP was similar to that in controls (30 degrees in both). Eyes with Brown syndrome and inverted Brown syndrome had lower maximal excyclorotation than in controls (10 and 20 vs. 30 degrees, respectively). Maximal incyclorotation in eyes with inverted Brown syndrome was lower than in controls (12.5 vs. 30 degrees), whereas it was similar to that of controls in eyes with presumed congenital SOP, acquired SOP, and Brown syndrome (30 degrees in each condition). Median maximal excyclorotation after SO disinsertion was 62.5 degrees, and maximal incyclorotation after IO disinsertion was 60 degrees. Photographic assessment yielded findings essentially identical to the surgeon's report. Test-retest reliability of the photographic reading was excellent, and agreement between the surgeon's report and the photographic reading was also excellent (95% limits of agreement, 4.4 and 11.6; intraclass correlation coefficient, 0.97 and 0.82, respectively).ConclusionsThe new torsional forced duction test enables quantitative assessment of SO and IO tightness and laxity.
| S-EPMC4549184 | biostudies-literature
Project description:Rats were anesthetized with sodium pentobarbital (50 mg/kg, i.p.) and placed in a stereotaxic instrument (Kopf instrument). After exposing the skull, bilateral craniotomy (0.5 - 0.8 mm holes, 4 mm posterior to bregma and 2.6 mm lateral from midline) was done. In one group of rats (Lactate group), each hippocampus (3.5 mm ventral from the surface of the skull at the craniotomy site) was infused with 100 nmol of L-lactate dissolved in 1µl of ACSF at a flow rate of 0.1 µl/min (controlled by microinjection pump; World Precision Instruments, USA). In another group of rats (ACSF group), 1 µl of artificial cerebrospinal fluid (ACSF; NaCl 124 mM, KCl 3 mM, CaCl2 2.4 mM, MgSO4 1.3 mM, glucose 10 mM, and HEPES 10 mM, pH = 7.3) was infused per HPC. Needle was kept at injection site for additional 5 minutes for the proper dispersion of solution after L-lactate/ACSF infusion. Then rats were kept into their cages for approximately 60 minutes. After that higher dose of sodium pentobarbital was given, and decapitation was done quickly. Following decapitation, the dura mater was removed carefully, and the brain was flipped out from skull into ice cold PBS using spatula. The right and left hippocampus were isolated on an ice-cold plate using sterile forceps and were stored immediately at -80°C until further use. Later, the right hippocampus was used as sample for mass spectrometry (MS).
2023-02-23 | PXD039121 | JPOST Repository
Project description:Individual differences in coping with stress may determine either a vulnerable or resilient phenotype. Therefore, it is important to better understand the biology underlying the behavioral phenotype. We assessed whether individual behavioral phenotype to acute stress is related with the hippocampal expression of glucocorticoid receptor (GR), Nurr1, interleukin-1 beta (IL-1β) or brain-derived neurotrophic factor (BDNF). Wistar male rats were exposed to forced swimming for 15 min and sacrificed at different times. Behavioral response was analyzed, and it was compared with the gene and protein expression of GR, Nurr1, IL-1β and BDNF in the hippocampus for each time point. Behavioral phenotyping showed a group with high immobility (vulnerable) while another had low immobility (resilient). No significant differences were found in the Nurr1, IL-1β and BDNF mRNA levels between resilient and vulnerable rats at different recovery times except for Nr3c1 (gene for GR). However, exposure to stress caused significantly higher levels of GR, Nurr1 and IL-1β proteins of vulnerable compared to resilient rats. This variability of behavioral phenotypes is associated with a differential molecular response to stress that involves GR, Nurr1, and IL-1β as mediators in coping with stress. This contributes to identifying biomarkers of susceptibility to stress.
| S-EPMC8657438 | biostudies-literature
Project description:We utilized ChIP Seq to examine the the genomic localization of the increase in H3K9 trimethylation we had previously observed in the hippocampus as a consequence of acute restraint stress in rats (Hunter et. al PNAS 2009). Rats were restrained for 30 minutes, allowed to recover for 1 hour and then sacrificed and their hippocampi extracted and processed for H3K9me3 ChIP using the Cell Signalling H3K9me3 antibody.
2012-11-02 | E-GEOD-41217 | biostudies-arrayexpress
Project description:Many immediate early genes (IEGs) have activity-dependent induction in a subset of brain subdivisions or neuron types. However, none have been reported yet with regulation specific to thalamic-recipient sensory neurons of the telencephalon or in the thalamic sensory input neurons themselves. Here, we report the first such gene, dual specificity phosphatase 1 (dusp1). Dusp1 is an inactivator of mitogen-activated protein kinase (MAPK), and MAPK activates expression of egr1, one of the most commonly studied IEGs, as determined in cultured cells. We found that in the brain of naturally behaving songbirds and other avian species, hearing song, seeing visual stimuli, or performing motor behavior caused high dusp1 upregulation, respectively, in auditory, visual, and somatosensory input cell populations of the thalamus and thalamic-recipient sensory neurons of the telencephalic pallium, whereas high egr1 upregulation occurred only in subsequently connected secondary and tertiary sensory neuronal populations of these same pathways. Motor behavior did not induce high levels of dusp1 expression in the motor-associated areas adjacent to song nuclei, where egr1 is upregulated in response to movement. Our analysis of dusp1 expression in mouse brain suggests similar regulation in the sensory input neurons of the thalamus and thalamic-recipient layer IV and VI neurons of the cortex. These findings suggest that dusp1 has specialized regulation to sensory input neurons of the thalamus and telencephalon; they further suggest that this regulation may serve to attenuate stimulus-induced expression of egr1 and other IEGs, leading to unique molecular properties of forebrain sensory input neurons.
| S-EPMC2904818 | biostudies-literature
Project description:The current study was aimed to investigate the correlations between immobility time in the forced swimming test (FST, a behavioral indicator of stress level) and hippocampal monoamine levels (markers of depression), plasma adrenalin level (a peripheral marker of stress) as well as fluoro-jade C staining (a marker of neurodegeneration).Male Sprague-Dawley rats were subjected to acute, sub-chronic (7 d) or chronic (14 d) FSTs and immobility time was recorded. Levels of noradrenalin, serotonin and dopamine in the hippocampus, and adrenalin level in the plasma were quantified by high-performance liquid chromatography with electrochemical detection. Brain sections from rats after chronic forced swimming or rotenone treatment (3 mg/kg subcutaneously for 4 d) were stained with fluoro-jade C.The rats subjected to swimming stress (acute, sub-chronic and chronic) showed long immobility times [(214 +/- 5), (220 +/- 4) and (231 +/- 7) s, respectively], indicating that the animals were under stress. However, the rats did not exhibit significant declines in hippocampal monoamine levels, and the plasma adrenalin level was not significantly increased compared to that in unstressed rats. The rats that underwent chronic swimming stress did not manifest fluoro-jade C staining in brain sections, while degenerating neurons were evident after rotenone treatment.The immobility time in the FST does not correlate with markers of depression (monoamine levels) and internal stress (adrenalin levels and neurodegeneration), hence this parameter may not be a true indicator of stress level.
| S-EPMC5560311 | biostudies-other
Project description:A fundamental issue in locomotion is to understand how muscle forcing produces apparently complex deformation kinematics leading to movement of animals like undulatory swimmers. The question of whether complicated muscle forcing is required to create the observed deformation kinematics is central to the understanding of how animals control movement. In this work, a forced damped oscillation framework is applied to a chain-link model for undulatory swimming to understand how forcing leads to deformation and movement. A unified understanding of swimming, caused by muscle contractions ("active" swimming) or by forces imparted by the surrounding fluid ("passive" swimming), is obtained. We show that the forcing triggers the first few deformation modes of the body, which in turn cause the translational motion. We show that relatively simple forcing patterns can trigger seemingly complex deformation kinematics that lead to movement. For given muscle activation, the forcing frequency relative to the natural frequency of the damped oscillator is important for the emergent deformation characteristics of the body. The proposed approach also leads to a qualitative understanding of optimal deformation kinematics for fast swimming. These results, based on a chain-link model of swimming, are confirmed by fully resolved computational fluid dynamics (CFD) simulations. Prior results from the literature on the optimal value of stiffness for maximum speed are explained.
| S-EPMC3681642 | biostudies-literature
Project description:Vagus nerve stimulation (VNS) has been shown to enhance learning and memory, yet the mechanisms behind these enhancements are unknown. We show that VNS altered the hippocampal, cortical, and blood epigenetic transcriptomes in male Sprague Dawley rats whether or not the rats performed a novelty preference behavioral task. In the hippocampus, novelty preference correlated with decreased histone deacetylase 11 (HDAC11), a transcriptional repressor enriched in CA1 cells important for memory consolidation. In the cortex, the immediate early gene (IEG) ARC was increased in VNS rats and correlated with transcription of plasticity genes and epigenetic regulators, including HDAC3. For rats performing the novelty preference task, ARC correlated with performance. Surprisingly, VNS did not significantly reduce transcription of cortical or hippocampal proinflammatory cytokines. However, TNFRSF11B (osteoprotegerin) correlated with novelty preference as well as plasticity, stress–response signaling, and epigenetic regulation in both hippocampus and cortex. Together, our findings provide the first evidence that VNS induces widespread changes in the cognitive epigenetic landscape and specifically affects epigenetic modulators associated with novelty preference, stress–response signaling, memory consolidation, and cortical neural remodeling.
2019-07-16 | GSE134309 | GEO