scholarly journals Short Daily Exposure to Environmental Enrichment, Fluoxetine, or Their Combination Reverses Deterioration of the Coat and Anhedonia Behaviors with Differential Effects on Hippocampal Neurogenesis in Chronically Stressed Mice

2021 ◽  
Vol 22 (20) ◽  
pp. 10976
Author(s):  
Gerardo Bernabé Ramírez-Rodríguez ◽  
Nelly Maritza Vega-Rivera ◽  
David Meneses-San Juan ◽  
Leonardo Ortiz-López ◽  
Erika Montserrat Estrada-Camarena ◽  
...  
Keyword(s):  
Pharmacological Treatment ◽  
Environmental Enrichment ◽  
Antidepressant Treatment ◽  
Antidepressant Drugs ◽  
Chronic Mild Stress ◽  
Living Environment ◽  
Hippocampal Neurogenesis ◽  
Mild Stress ◽  
Daily Exposure ◽  
Newborn Neurons

Depression is a neuropsychiatric disorder with a high impact on the worldwide population. To overcome depression, antidepressant drugs are the first line of treatment. However, pre-clinical studies have pointed out that antidepressants are not entirely efficacious and that the quality of the living environment after stress cessation may play a relevant role in increasing their efficacy. As it is unknown whether a short daily exposure to environmental enrichment during chronic stress and antidepressant treatment will be more effective than just the pharmacological treatment, this study analyzed the effects of fluoxetine, environmental enrichment, and their combination on depressive-associated behavior. Additionally, we investigated hippocampal neurogenesis in mice exposed to chronic mild stress. Our results indicate that fluoxetine reversed anhedonia. Besides, fluoxetine reversed the decrement of some events of the hippocampal neurogenic process caused by chronic mild stress. Conversely, short daily exposure to environmental enrichment changed the deterioration of the coat and anhedonia. Although, this environmental intervention did not produce significant changes in the neurogenic process affected by chronic mild stress, fluoxetine plus environmental enrichment showed similar effects to those caused by environmental enrichment to reverse depressive-like behaviors. Like fluoxetine, the combination reversed the declining number of Ki67, doublecortin, calretinin cells and mature newborn neurons. Finally, this study suggests that short daily exposure to environmental enrichment improves the effects of fluoxetine to reverse the deterioration of the coat and anhedonia in chronically stressed mice. In addition, the combination of fluoxetine with environmental enrichment produces more significant effects than those caused by fluoxetine alone on some events of the neurogenic process. Thus, environmental enrichment improves the benefits of pharmacological treatment by mechanisms that need to be clarified.

scholarly journals Changes in the functional connectome and behavior after exposure to chronic stress and increasing neurogenesis

2020 ◽  
Author(s):  
Luka Culig ◽  
Patrick E. Steadman ◽  
Justin W. Kenney ◽  
Sandra Legendre ◽  
Frédéric Minier ◽  
...  
Keyword(s):  
Chronic Stress ◽  
Granule Cells ◽  
Brain Networks ◽  
Chronic Mild Stress ◽  
Protective Role ◽  
Hippocampal Neurogenesis ◽  
Adult Hippocampal Neurogenesis ◽  
Mild Stress ◽  
Brain Circuitry ◽  
Newborn Neurons

AbstractAddition of new neurons to the dentate gyrus might change the activity of neural circuitry in the areas which the hippocampus projects to. The size of the hippocampus and the number of adult newborn granule cells are decreased by unpredictable chronic mild stress (UCMS). Additionally, one of the notable effects of chronic stress is the induction of ΔFosB, an unusually stable transcription factor which accumulates over time in several brain areas. This accumulation has been observed in many animal models of depression and it could have a protective role against stress, but no studies so far have explored how a specific increase in neurogenesis might regulate the induction and which brain networks might be predominately affected.We attempted to investigate the role of increasing adult hippocampal neurogenesis on stress-related behavior and the functional brain circuitry involved in mice exposed to UCMS. We used iBax mice, in which the pro-apoptotic gene Bax can be selectively ablated in neural stem cells, therefore inducibly enhancing survival of newborn neurons after tamoxifen administration. The animals were exposed to UCMS for 9 weeks and treated with tamoxifen in week 3 after the beginning of UCMS. In week 8, they were submitted to a battery of behavioral tests to assess depressive-like and anxiety-like behavior. In week 9, blood was collected to assess basal corticosterone levels, and the animals were sacrificed and their brain collected for ΔFosB immunohistochemistry. Brain-wide maps of ΔFosB expression were constructed and graph theoretical analyses were used to study the changes in brain networks after stress.UCMS induced negative correlations between the lateral entorhinal cortex and both the hippocampal structures and the nucleus accumbens in the VEH-treated mice, which were not present in other groups. Ranking nodes by degree reveals a strong thalamic-cortical signature in both non-stress (NS) groups. Exposure to UCMS seems to induce activity in thalamic areas and cerebral nuclei, with a different signature in the UCMS TAM group, which seems to completely “disengage” the neocortex and has most of its nodes with the most connections in the thalamic areas.

Region-dependent and stage-specific effects of stress, environmental enrichment, and antidepressant treatment on hippocampal neurogenesis

Hippocampus ◽  
2013 ◽  
Vol 23 (9) ◽  
pp. 797-811 ◽  
Author(s):  
Arnaud Tanti ◽  
Willy-Paul Westphal ◽  
Virginie Girault ◽  
Bruno Brizard ◽  
Severine Devers ◽  
...  
Keyword(s):  
Environmental Enrichment ◽  
Antidepressant Treatment ◽  
Hippocampal Neurogenesis ◽  
Specific Effects ◽  
Effects Of Stress

scholarly journals Role of AC-cAMP-PKA Cascade in Antidepressant Action of Electroacupuncture Treatment in Rats

2012 ◽  
Vol 2012 ◽  
pp. 1-7 ◽  
Author(s):  
Jian-hua Liu ◽  
Zhi-feng Wu ◽  
Jian Sun ◽  
Li Jiang ◽  
Shuo Jiang ◽  
...  
Keyword(s):  
Signal Transduction ◽  
Antidepressant Treatment ◽  
Signal Transduction Pathway ◽  
Cyclic Adenosine Monophosphate ◽  
Chronic Mild Stress ◽  
Adenosine Monophosphate ◽  
Mild Stress ◽  
Transduction Pathway ◽  
Antidepressant Action

Adenylyl cyclase (AC)-cyclic adenosine monophosphate (cAMP)-cAMP-dependent protein kinase A (PKA) cascade is considered to be associated with the pathogenesis and treatment of depression. The present study was conducted to explore the role of the cAMP cascade in antidepressant action of electroacupuncture (EA) treatment for chronic mild stress (CMS)-induced depression model rats. The results showed that EA improved significantly behavior symptoms in depression and dysfunction of AC-cAMP-PKA signal transduction pathway induced by CMS, which was as effective as fluoxetine. Moreover, the antidepressant effects of EA rather than Fluoxetine were completely abolished by H89, a specific PKA inhibitor. Consequently, EA has a significant antidepressant treatment in CMS-induced depression model rats, and AC-cAMP-PKA signal transduction pathway is crucial for it.

scholarly journals The Neural Plasticity Theory of Depression: Assessing the Roles of Adult Neurogenesis and PSA-NCAM within the Hippocampus

2013 ◽  
Vol 2013 ◽  
pp. 1-14 ◽  
Author(s):  
Steven R. Wainwright ◽  
Liisa A. M. Galea
Keyword(s):  
Neural Plasticity ◽  
Brain Plasticity ◽  
Antidepressant Treatment ◽  
Antidepressant Drugs ◽  
Hippocampal Neurogenesis ◽  
Adult Hippocampal Neurogenesis ◽  
Neural Structure ◽  
Treatment Of Depression ◽  
Prevalent Disease ◽  
And Function

Depression is a devastating and prevalent disease, with profound effects on neural structure and function; however the etiology and neuropathology of depression remain poorly understood. Though antidepressant drugs exist, they are not ideal, as only a segment of patients are effectively treated, therapeutic onset is delayed, and the exact mechanism of these drugs remains to be elucidated. Several theories of depression do exist, including modulation of monoaminergic neurotransmission, alterations in neurotrophic factors, and the upregulation of adult hippocampal neurogenesis, and are briefly mentioned in the review. However none of these theories sufficiently explains the pathology and treatment of depression unto itself. Recently, neural plasticity theories of depression have postulated that multiple aspects of brain plasticity, beyond neurogenesis, may bridge the prevailing theories. The term “neural plasticity” encompasses an array of mechanisms, from the birth, survival, migration, and integration of new neurons to neurite outgrowth, synaptogenesis, and the modulation of mature synapses. This review critically assesses the role of adult hippocampal neurogenesis and the cell adhesion molecule, PSA-NCAM (which is known to be involved in many facets of neural plasticity), in depression and antidepressant treatment.

scholarly journals Chronic mild stress and antidepressant treatment alter 5-HT1A receptor expression by modifying DNA methylation of a conserved Sp4 site

2015 ◽  
Vol 82 ◽  
pp. 332-341 ◽  
Author(s):  
Brice Le François ◽  
Jeremy Soo ◽  
Anne M. Millar ◽  
Mireille Daigle ◽  
Anne-Marie Le Guisquet ◽  
...  
Keyword(s):  
Dna Methylation ◽  
Antidepressant Treatment ◽  
Chronic Mild Stress ◽  
Receptor Expression ◽  
Mild Stress
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