scholarly journals Fluoxetine effects on behavior and adult hippocampal neurogenesis in female C57BL/6J mice across the estrous cycle

2018 ◽  
Author(s):  
Christine N. Yohn ◽  
Sophie Shifman ◽  
Alexander Garino ◽  
Emma Diethorn ◽  
Leshya Bokka ◽  
...  
Keyword(s):  
Estrous Cycle ◽  
Antidepressant Treatment ◽  
Hippocampal Neurogenesis ◽  
Adult Hippocampal Neurogenesis ◽  
List Type ◽  
Female Mice ◽  
Chronic Fluoxetine ◽  
Brain And Behavior ◽  
And Behavior ◽  
The Impact

AbstractSome mood disorders, such as major depressive disorder, are more prevalent in women than in men. However, historically preclinical studies in rodents have a lower inclusion rate of females than males, possibly due to the fact that behavior can be affected by the estrous cycle. Several studies have demonstrated that chronic antidepressant treatment can decrease anxiety-like behaviors and increase adult hippocampal neurogenesis in male rodents. However, very few studies have conclusively looked at the effects of antidepressants on behavior and neurogenesis across the estrous cycle in naturally cycling female rodents. Here we analyze the effects of chronic treatment with the selective serotonin reuptake inhibitor (SSRI) fluoxetine (Prozac) on behavior and adult hippocampal neurogenesis in naturally cycling C57BL/6J females across all four phases of the estrous cycle. Interestingly, we find that the effects of fluoxetine on both behavior and adult hippocampal neurogenesis are driven by mice specifically in the estrus or diestrus phases of the estrous cycle. Taken together our data is the first to illustrate the impact of fluoxetine on brain and behavior across all four stages of the murine estrous cycle.HighlightsChronic fluoxetine reduces anxiety-like behaviors in naturally cycling female miceChronic fluoxetine increases adult hippocampal neurogenesis in naturally cycling female miceThe effects of chronic fluoxetine on behavior and adult hippocampal neurogenesis are driven by the estrus and diestrus phases of the estrous cycle

scholarly journals Social Instability is an Effective Chronic Stress Paradigm for both Male and Female Mice

2019 ◽  
Author(s):  
Christine N. Yohn ◽  
Sandra A. Ashamalla ◽  
Leshya Bokka ◽  
Mark M. Gergues ◽  
Alexander Garino ◽  
...  
Keyword(s):  
Chronic Stress ◽  
Hpa Axis ◽  
Social Stress ◽  
Antidepressant Treatment ◽  
Hippocampal Neurogenesis ◽  
Adult Hippocampal Neurogenesis ◽  
Social Instability ◽  
Female Mice ◽  
Negative Valence ◽  
Males And Females

ABSTRACTDespite stress-associated disorders having a higher incidence rate in females, preclinical research mainly focuses on males. Chronic stress paradigms, such as chronic social defeat and chronic corticosterone administration, were mainly designed and validated in males and subsequent attempts to use these paradigms in females has demonstrated sex differences in the behavioral and HPA axis response to stress. Here, we developed a social stress paradigm, social instability stress (SIS), which exposes adult mice to unstable social hierarchies for 7 weeks. SIS effectively induces negative valence behaviors and hypothalamus-pituitary-adrenal (HPA) axis activation in both males and females. Importantly, while there were effects of estrous cycle on behavior, this variability did not impact the overall effects of SIS on behavior, suggesting estrous does not need to be tracked while utilizing SIS. Furthermore, the effects of SIS on negative valence behaviors were also reversed following chronic antidepressant treatment with fluoxetine (FLX) in both males and females. SIS also reduced adult hippocampal neurogenesis in female mice, while chronic FLX treatment increased adult hippocampal neurogenesis in both males and females. Overall, these data demonstrate that the SIS paradigm is an ethologically valid approach that effectively induces chronic stress in both adult male and adult female mice.

scholarly journals Selective increases in inter-individual variability in response to environmental enrichment in female mice

eLife ◽  
2018 ◽  
Vol 7 ◽  
Author(s):  
Julia C Körholz ◽  
Sara Zocher ◽  
Anna N Grzyb ◽  
Benjamin Morisse ◽  
Alexandra Poetzsch ◽  
...  
Keyword(s):  
Environmental Enrichment ◽  
Specific Activity ◽  
Individual Variability ◽  
Hippocampal Neurogenesis ◽  
Adult Hippocampal Neurogenesis ◽  
Multiple Parameters ◽  
Wide Range ◽  
Suitable Animal Model ◽  
Brain And Behavior ◽  
And Behavior

One manifestation of individualization is a progressively differential response of individuals to the non-shared components of the same environment. Individualization has practical implications in the clinical setting, where subtle differences between patients are often decisive for the success of an intervention, yet there has been no suitable animal model to study its underlying biological mechanisms. Here we show that enriched environment (ENR) can serve as a model of brain individualization. We kept 40 isogenic female C57BL/6JRj mice for 3 months in ENR and compared these mice to an equally sized group of standard-housed control animals, looking at the effects on a wide range of phenotypes in terms of both means and variances. Although ENR influenced multiple parameters and restructured correlation patterns between them, it only increased differences among individuals in traits related to brain and behavior (adult hippocampal neurogenesis, motor cortex thickness, open field and object exploration), in agreement with the hypothesis of a specific activity-dependent development of brain individuality.

scholarly journals Selective increases in inter-individual variability in response to environmental enrichment

2018 ◽  
Author(s):  
Julia Körholz ◽  
Sara Zocher ◽  
Anna N. Grzyb ◽  
Benjamin Morisse ◽  
Alexandra Poetzsch ◽  
...  
Keyword(s):  
Environmental Enrichment ◽  
Specific Activity ◽  
Individual Variability ◽  
Hippocampal Neurogenesis ◽  
Adult Hippocampal Neurogenesis ◽  
Multiple Parameters ◽  
Wide Range ◽  
Suitable Animal Model ◽  
Brain And Behavior ◽  
And Behavior

AbstractOne manifestation of individualization is a progressively differential response of individuals to the non-shared components of the same environment. Individualization has practical implications in clinical setting, where subtle differences between patients are often decisive for the success of an intervention, yet there has been no suitable animal model to study its underlying biological mechanisms. Here we show that enriched environment (ENR) can serve as a model of brain individualization. We kept 40 isogenic mice for 3 months in ENR and compared the effects on a wide range of phenotypes on both mean and variance to an equally sized group of standard-housed control animals. While ENR influenced multiple parameters and restructured correlation patterns between them, it only increased differences among individuals in traits related to brain and behavior (adult hippocampal neurogenesis, motor cortex thickness, open field and object exploration, rotarod performance), in agreement with the hypothesis of a specific activity-dependent development of brain individuality.

scholarly journals A non-linear relation between levels of adult hippocampal neurogenesis and expression of the immature neuron marker doublecortin

2020 ◽  
Author(s):  
Indira Mendez-David ◽  
Denis J David ◽  
Claudine Deloménie ◽  
Jean-Martin Beaulieu ◽  
Alain M. Gardier ◽  
...  
Keyword(s):  
Mouse Model ◽  
Chronic Stress ◽  
Granule Cells ◽  
Antidepressant Treatment ◽  
Hippocampal Neurogenesis ◽  
Neural Progenitors ◽  
Adult Hippocampal Neurogenesis ◽  
List Type ◽  
Stress Model ◽  
Immature Neuron

ABSTRACTWe investigated the mechanisms underlying the effects of the antidepressant fluoxetine on behavior and adult hippocampal neurogenesis (AHN). After confirming our earlier report that the signaling molecule β2-arrestin is required for the antidepressant-like effects of fluoxetine, we found that the effects of fluoxetine on proliferation of neural progenitors and on survival of adult-born granule cells are absent in the β2-arrestin knockout (β2-Arr KO) mice. To our surprise fluoxetine induced a dramatic upregulation of doublecortin (DCX) in the β2-Arr KO mice, indicating that DCX expression can be increased even though AHN is not. We discovered two other conditions where DCX expression is regulated non linearly compared to levels of AHN: a chronic stress model where DCX is upregulated and an inflammation model where DCX is down regulated. We conclude that assessing DCX expression alone to quantify levels of AHN can be misleading and that caution should be applied when label retention techniques are not available.HIGHLIGHTSβ2-arrestin (β-Arr2) is required for the antidepressant-like effects of fluoxetine.A dramatic upregulation of doublecortin (DCX) is observed in the β2-Arr KO mice after antidepressant treatment whereas its effects on proliferation of neural progenitors and on survival of adult-born granule cells are absent.DCX is more upregulated than the number of young neurons in a mouse model of depression.DCX is more down regulated than the number of young neurons in a model of inflammation.microRNAs (miRs) may contribute to the regulation of DCX mRNA expression.

FC29-02 - Is prenatal exposure to alcohol a factor which re-program the brain?

2011 ◽  
Vol 26 (S2) ◽  
pp. 1978-1978
Author(s):  
J.H. Sliwowska
Keyword(s):  
Prenatal Exposure ◽  
Hpa Axis ◽  
Alcohol Exposure ◽  
Hippocampal Neurogenesis ◽  
Adult Hippocampal Neurogenesis ◽  
Ovariectomized Rats ◽  
List Type ◽  
Depression And Anxiety ◽  
Hpg Axis ◽  
The Brain

IntroductionFetal programming refers to the concept that early environmental factors, including prenatal exposure to stress and drugs, can permanently organize or imprint physiological and behavioural systems and increase vulnerability to disorders such as depression and anxiety later in life.AimsIs prenatal exposure to alcohol a factor which re-programs the brain?ObjectivesEffects of prenatal alcohol exposure (PAE) on:1)the hypothalamus-pituitary-adrenal (HPA) axis;2)the hypothalamus-pituitary-gonadal (HPG) axis;3)serotonergic (5-HT) system and4)adult hippocampal neurogenesis are presented.MethodsOffspring from prenatal ethanol (PAE), pair-fed (PF) and ad lib-fed control (C) dams are studied across the development or in adulthood. Immunocytochemistry and in situ hybridization techniques are used.ResultsIn term of the HPA axis: PAE alters the balance of mineralocorticoids/glucocorticoids (MRs/GRs) receptor levels in the hippocampus of adult females. In the case of the HPG axis: PAE delays puberty and changes hormonal profiles in males and females. PAE also decreases numbers of 5-HT-immunoreactive neurons in the dorsal raphe nucleus of the brainstem in ovariectomized rats and estradiol and progesterone modulate those effects. Finally, in adult PAE males, but not females stress-induced decrease in neurogenesis is altered.ConclusionsIn our animal model PAE re-programs the brain. Effects of PAE are long-lasting, affect HPA and HPG axes, 5-HT system and adult hippocampal neurogenesis and if seen in humans could contribute to increased vulnerability to depression and anxiety.

scholarly journals Fluoxetine effects on behavior and adult hippocampal neurogenesis in female C57BL/6J mice across the estrous cycle

2020 ◽  
Vol 237 (5) ◽  
pp. 1281-1290 ◽  
Author(s):  
Christine N. Yohn ◽  
Sophie Shifman ◽  
Alexander Garino ◽  
Emma Diethorn ◽  
Leshya Bokka ◽  
...  
Keyword(s):  
Estrous Cycle ◽  
Hippocampal Neurogenesis ◽  
Adult Hippocampal Neurogenesis

scholarly journals Prenatal Developmental Origins of Future Psychopathology: Mechanisms and Pathways

2019 ◽  
Vol 15 (1) ◽  
pp. 317-344 ◽  
Author(s):  
Catherine Monk ◽  
Claudia Lugo-Candelas ◽  
Caroline Trumpff
Keyword(s):  
Maternal Distress ◽  
Developmental Origins ◽  
Neurodevelopmental Outcomes ◽  
Fetal Origins ◽  
Behavior Development ◽  
Increased Risk ◽  
Health And Disease ◽  
Brain And Behavior ◽  
And Behavior ◽  
The Impact

The developmental origins of health and disease hypothesis applied to neurodevelopmental outcomes asserts that the fetal origins of future development are relevant to mental health. There is a third pathway for the familial inheritance of risk for psychiatric illness beyond shared genes and the quality of parental care: the impact of pregnant women's distress—defined broadly to include perceived stress, life events, depression, and anxiety—on fetal and infant brain–behavior development. We discuss epidemiological and observational clinical data demonstrating that maternal distress is associated with children's increased risk for psychopathology: For example, high maternal anxiety is associated with a twofold increase in the risk of probable mental disorder in children. We review several biological systems hypothesized to be mechanisms by which maternal distress affects fetal and child brain and behavior development, as well as the clinical implications of studies of the developmental origins of health and disease that focus on maternal distress. Development and parenting begin before birth.

The Impact of Sodium Fluoride on Reproductive Function of Female Mice and Behavior of the Offspring

2014 ◽  
Vol 2014 (1) ◽  
pp. 2137
Author(s):  
Jian Zhou* ◽  
Honghui Li ◽  
Lingqin Zhu ◽  
Huifang Yang ◽  
Yanhong Cui ◽  
...  
Keyword(s):  
Sodium Fluoride ◽  
Reproductive Function ◽  
Female Mice ◽  
And Behavior ◽  
The Impact

scholarly journals Gonadal steroids, brain, and behavior: role of context

2002 ◽  
Vol 4 (2) ◽  
pp. 123-137 ◽  
Keyword(s):  
Mood Disorders ◽  
Steroid Hormones ◽  
Differential Susceptibility ◽  
Reproductive Function ◽  
Gonadal Steroids ◽  
Wide Range ◽  
Reproductive Endocrine ◽  
Brain And Behavior ◽  
And Behavior ◽  
The Impact

The nature and extent of the impact of gender and reproductive function on mood has been the subject of speculation and controversy for centuries. Over the past 50 years, however, it has become increasingly clear that not only is the brain a major target of reproductive steroid hormones, but additionally, the steroid hormones, as neuroregulators, create a context thai influences a broad range of brain activities; ie, neural actions and resultant behaviors are markedly different in the presence and absence of gonadal steroids. In turn, the actions of gonadal steroids are themselves context-dependent. Thus, even where it can be demonstrated thai gonadal steroids trigger mood disorders, the triggers are normal levels of gonadal steroids (to be contrasted with the mood disturbances accompanying endocrinopathies), and the mood disorders appear only in a subset of susceptible individuals. The context specificity and differential susceptibility to affective dysregulation seen in women with reproductive endocrine-related mood disorders are undoubtedly important underlying characteristics of a wide range of psychiatric disorders in which the triggers have not yet been identified. Consequently, reproductive endocrine-related mood disorders offer unparalleled promise for the identification of those contextual variables that permit biological stimuli to differentially translate into depression in individuals at risk.

Sign in / Sign up

Export Citation Format

Share Document