Behavioral and molecular alterations in mice resulting from chronic treatment with dexamethasone: Relevance to depression

Skupio, Urszula; Tertil, Magdalena; Sikora, Magdalena; Gołda, Sławomir; Wawrzczak-Bargieła, Agnieszka; Przewłocki, Ryszard

doi:10.1016/j.neuroscience.2014.11.035

Cited by 61 publications

(43 citation statements)

References 63 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…For example, in recent studies, the GLT‐1 protein levels are significantly reduced in the hippocampus of rats subjected to 35 or 42 days of CUS, accompanied by depression‐ and anxiety‐like behaviors in sucrose preference, forced swimming (FST) and open field tests (Chen et al, ; Liu et al, ). These findings are consistent with several other studies in which chronic exposure to corticosteroid or dexamethasone (a synthetic glucocorticoid) leads to a significant reduction in the levels of GLT‐1 and GLAST proteins and mRNAs in the mouse PFC and hippocampus (Gourley, Espitia, Sanacora, & Taylor, ; Skupio et al, ). In a chronic learned helplessness rat model of depression, helpless animals showed a significant decrease in GLT‐1 expression in the hippocampus and cerebral cortex compared with control littermates (Zink et al, ).…”

Section: Glutamate Homeostasissupporting

confidence: 92%

“…In rodent disease models of depression and anxiety (Yan, Cao, Das, Zhu, & Gao, ), alterations in components of the glutamate‐glutamine shuttle have always been noted; however, the findings vary, possibly due to the use of different experimental paradigms (Reagan et al, ; Sanacora and Banasr, ; Skupio et al, ; Wood, Young, Reagan, Chen, & McEwen, ; Yang, Huang, & Hsu, ; Zink, Vollmayr, Gebicke‐Haerter, & Henn, ). For example, in recent studies, the GLT‐1 protein levels are significantly reduced in the hippocampus of rats subjected to 35 or 42 days of CUS, accompanied by depression‐ and anxiety‐like behaviors in sucrose preference, forced swimming (FST) and open field tests (Chen et al, ; Liu et al, ).…”

Section: Glutamate Homeostasismentioning

confidence: 99%

See 1 more Smart Citation

An astroglial basis of major depressive disorder? An overview

Wang

Jie

Liu

et al. 2017

Glia

173

125

View full text Add to dashboard Cite

Depression is a chronic, recurring, and serious mood disorder that afflicts up to 20% of the global population. The monoamine hypothesis has dominated our understanding of the pharmacotherapy of depression for more than half a century; however, our understanding of the pathophysiology and pathogenesis of major depression has lagged far behind. Astrocytes are the most abundant and versatile cells in the brain, participating in most, if not all, of brain functions as both a passive housekeeper and an active player. Mounting evidence from clinical, preclinical and post-mortem studies has revealed a decrease in the number or density of astrocytes and morphological and functional astroglial atrophy in patients with major depressive disorder (MDD) and in animal models of depression. Furthermore, currently available antidepressant treatments at least partially exert their therapeutic effects on astrocytes. More importantly, dysfunctional astrocytes lead to depressive-like phenotypes in animals. Together, current studies point to astroglial pathology as the potential root cause of MDD. Thus, a shift from a neuron-centric to an astrocyte-centric cause of MDD has gained increasing attention during the past two decades. Here we will summarize the current evidence supporting the hypothesis that MDD is a disease of astrocyte pathology and highlight previous studies on promising strategies that directly target astrocytes for the development of novel antidepressant treatments.

show abstract

Section: Glutamate Homeostasissupporting

confidence: 92%

Section: Glutamate Homeostasismentioning

confidence: 99%

An astroglial basis of major depressive disorder? An overview

Wang

Jie

Liu

et al. 2017

Glia

173

125

View full text Add to dashboard Cite

show abstract

“…Notably, the regulation of EGR1 expression by SGK1 involves well-defined mechanisms of Egr1 transcriptional regulation via the activation by phosphorylation of SRF and CREB, and has been linked to spatial memory formation in rats (Tyan et al, 2008). As its expression in the rodent hippocampus and mPFC rodents is strongly regulated by acute (Bohacek et al, 2015; Mifsud and Reul, 2016) or chronic stress (Anacker et al, 2013; Miyata et al, 2015; Skupio et al, 2015; Cattaneo and Riva, 2016; Wei et al, 2016), SGK1 emerges as a particularly interesting candidate in mediating EGR1 regulations in response to various stress paradigms. In this context, it is particularly interesting to note that SGK1 expression levels are down-regulated in the PFC of post-traumatic stress disorder patients—or increased in the peripheral blood of unmedicated depressed patients (Anacker et al, 2013)—and that SGK1 inhibition in the rat mPFC induces depressive-like behaviors in rodents associated with abnormal dendritic spine morphology and synaptic dysfunction (Licznerski et al, 2015).…”

Section: Egr1 Role In Pathological Statesmentioning

confidence: 99%

The Role of Early Growth Response 1 (EGR1) in Brain Plasticity and Neuropsychiatric Disorders

Duclot

Kabbaj

2017

Front. Behav. Neurosci.

267

240

View full text Add to dashboard Cite

It is now clearly established that complex interactions between genes and environment are involved in multiple aspects of neuropsychiatric disorders, from determining an individual’s vulnerability to onset, to influencing its response to therapeutic intervention. In this perspective, it appears crucial to better understand how the organism reacts to environmental stimuli and provide a coordinated and adapted response. In the central nervous system, neuronal plasticity and neurotransmission are among the major processes integrating such complex interactions between genes and environmental stimuli. In particular, immediate early genes (IEGs) are critical components of these interactions as they provide the molecular framework for a rapid and dynamic response to neuronal activity while opening the possibility for a lasting and sustained adaptation through regulation of the expression of a wide range of genes. As a result, IEGs have been tightly associated with neuronal activity as well as a variety of higher order processes within the central nervous system such as learning, memory and sensitivity to reward. The immediate early gene and transcription factor early growth response 1 (EGR1) has thus been revealed as a major mediator and regulator of synaptic plasticity and neuronal activity in both physiological and pathological conditions. In this review article, we will focus on the role of EGR1 in the central nervous system. First, we will summarize the different factors influencing its activity. Then, we will analyze the amount of data, including genome-wide, that has emerged in the recent years describing the wide variety of genes, pathways and biological functions regulated directly or indirectly by EGR1. We will thus be able to gain better insights into the mechanisms underlying EGR1’s functions in physiological neuronal activity. Finally, we will discuss and illustrate the role of EGR1 in pathological states with a particular interest in cognitive functions and neuropsychiatric disorders.

show abstract

“…Next, to demonstrate the potential of SIM imaging, we analyzed spine forms in chronic Dex‐treated mice. Chronic treatment with Dex, an agonist of the glucocorticoid receptor, is known to induce depression‐like behaviors in rodents (Casarotto & Andreatini, ; Sigwalt et al ., ; Skupio et al ., ); accordingly, pyramidal neurons in the mPFC are expected to atrophy as in other mouse models of depression (Cerqueira et al ., ; Banasr et al ., ; Duman & Duman, ). In L5PNs, atrophy has been observed in the tips, but not the main shaft, of apical dendrites.…”

Section: Resultsmentioning

confidence: 96%

Super‐resolution structural analysis of dendritic spines using three‐dimensional structured illumination microscopy in cleared mouse brain slices

Sawada

Kawakami

Shigemoto

et al. 2018

Eur J of Neuroscience

View full text Add to dashboard Cite

Three‐dimensional (3D) super‐resolution microscopy technique structured illumination microscopy (SIM) imaging of dendritic spines along the dendrite has not been previously performed in fixed tissues, mainly due to deterioration of the stripe pattern of the excitation laser induced by light scattering and optical aberrations. To address this issue and solve these optical problems, we applied a novel clearing reagent, LUCID, to fixed brains. In SIM imaging, the penetration depth and the spatial resolution were improved in LUCID‐treated slices, and 160‐nm spatial resolution was obtained in a large portion of the imaging volume on a single apical dendrite. Furthermore, in a morphological analysis of spine heads of layer V pyramidal neurons (L5PNs) in the medial prefrontal cortex (mPFC) of chronic dexamethasone (Dex)‐treated mice, SIM imaging revealed an altered distribution of spine forms that could not be detected by high‐NA confocal imaging. Thus, super‐resolution SIM imaging represents a promising high‐throughput method for revealing spine morphologies in single dendrites.

show abstract

Behavioral and molecular alterations in mice resulting from chronic treatment with dexamethasone: Relevance to depression

Cited by 61 publications

References 63 publications

An astroglial basis of major depressive disorder? An overview

An astroglial basis of major depressive disorder? An overview

The Role of Early Growth Response 1 (EGR1) in Brain Plasticity and Neuropsychiatric Disorders

Super‐resolution structural analysis of dendritic spines using three‐dimensional structured illumination microscopy in cleared mouse brain slices

Contact Info

Product

Resources

About