Eszopiclone Facilitation of Fluoxetine Treatment Using a Social Defeat Model

2009 ◽  
Author(s):  
Jessica J. Smith ◽  
Daniel M. Noel ◽  
Meredith L. Smith ◽  
A. Brianna Sheppard ◽  
Russell W. Brown
Keyword(s):  
Social Defeat ◽  
Fluoxetine Treatment

scholarly journals Effects of social defeat stress and fluoxetine treatment on neurogenesis and behaviour in mice that lack zinc transporter 3 (ZnT3) and vesicular zinc

2019 ◽  
Author(s):  
Brendan B. McAllister ◽  
Angela Pochakom ◽  
Selena Fu ◽  
Richard H. Dyck
Keyword(s):  
Knockout Mice ◽  
Selective Serotonin Reuptake Inhibitors ◽  
Social Defeat ◽  
Zinc Transporter ◽  
Hippocampal Neurogenesis ◽  
Adult Hippocampal Neurogenesis ◽  
Social Avoidance ◽  
Wild Type ◽  
Social Defeat Stress ◽  
Fluoxetine Treatment

ABSTRACTDepression is a leading cause of disability worldwide, in part because the available treatments are inadequate and do not work for many people. The neurobiology of depression, and the mechanism of action of common antidepressant drugs such as selective serotonin reuptake inhibitors (SSRIs), is not well understood. One mechanism thought to underlie the effects of these drugs is upregulation of adult hippocampal neurogenesis. Evidence indicates that vesicular zinc is required for modulation of adult hippocampal neurogenesis, at least under some circumstances. Vesicular zinc refers to zinc that is stored in the synaptic vesicles of certain neurons, including in the hippocampus, and released in response to neuronal activity. It can be eliminated from the brain by deletion of zinc transporter 3 (ZnT3), as is the case in ZnT3 knockout mice. Here, we examined the effects of repeated social defeat stress and subsequent chronic treatment with the SSRI fluoxetine on behaviour and neurogenesis in ZnT3 knockout mice. We hypothesized that fluoxetine treatment would increase neurogenesis and reverse stress-induced behavioural symptoms in wild type, but not ZnT3 knockout, mice. As anticipated, stress induced persistent depression-like effects, including social avoidance and anxiety-like behaviour. Fluoxetine decreased social avoidance, though the effect was not specific to the stressed mice, but did not affect anxiety-like behaviour. Surprisingly, stress increased the survival of neurons born 1 day after the last episode of defeat stress. Fluoxetine treatment also increased cell survival, particularly in wild type mice, though it did not affect proliferation. Our results did not support our hypothesis that vesicular zinc is required for the behavioural benefits of fluoxetine treatment. As to whether vesicular zinc is required for the neurogenic effects of fluoxetine, our results were inconclusive, warranting further investigation into the role of vesicular zinc in adult hippocampal neurogenesis.

Strain-specific outcomes of repeated social defeat and chronic fluoxetine treatment in the mouse

2011 ◽  
Vol 97 (3) ◽  
pp. 566-576 ◽  
Author(s):  
Maria Razzoli ◽  
Lucia Carboni ◽  
Michela Andreoli ◽  
Francesca Michielin ◽  
Alice Ballottari ◽  
...  
Keyword(s):  
Social Defeat ◽  
Fluoxetine Treatment ◽  
Chronic Fluoxetine

The impact of social defeat on cardiac activity in rats

1998 ◽  
Author(s):  
A. Sgoifo ◽  
S. F. de Boer ◽  
B. Buwalda ◽  
F. Maes ◽  
J. M. Koolhaas
Keyword(s):  
Cardiac Activity ◽  
Social Defeat ◽  
The Impact

Altered myeloid and lymphoid immune cell responses following repeated social defeat stress

2015 ◽  
Vol 48 (06) ◽  
Author(s):  
O Ambree ◽  
C Ruland ◽  
P Zwanzger ◽  
V Arolt ◽  
J Alferink
Keyword(s):  
Immune Cell ◽  
Social Defeat ◽  
Social Defeat Stress ◽  
Cell Responses

Our Most Troubling Madness

2016 ◽  
Keyword(s):  
Social Defeat ◽  
Social World ◽  
Epidemiological Evidence ◽  
The West ◽  
Social Settings ◽  
The Social ◽  
Brain Alteration ◽  
Benign Course ◽  
Cultural Features ◽  
The Way

This book examines the way schizophrenia is shaped by its social context: how life is lived with this madness in different settings, and what it is about those settings that alters the course of the illness, its outcome, and even the structure of its symptoms. Until recently, schizophrenia was perhaps our best example—our poster child—for the “bio-bio-bio” model of psychiatric illness: genetic cause, brain alteration, pharmacologic treatment. We now have direct epidemiological evidence that people are more likely to fall ill with schizophrenia in some social settings than in others, and more likely to recover in some social settings than in others. Something about the social world gets under the skin. This book presents twelve case studies written by psychiatric anthropologists that help to illustrate some of the variability in the social experience of schizophrenia and that illustrate the main hypotheses about the different experience of schizophrenia in the west and outside the west--and in particular, why schizophrenia seems to have a more benign course and outcome in India. We argue that above all it is the experience of “social defeat” that increases the risk and burden of schizophrenia, and that opportunities for social defeat are more abundant in the modern west. There is a new role for anthropology in the science of schizophrenia. Psychiatric science has learned—epidemiologically, empirically, quantitatively—that our social world makes a difference. But the highly structured, specific-variable analytic methods of standard psychiatric science cannot tell us what it is about culture that has that impact. The careful observation enabled by rich ethnography allows us to see in more detail what kinds of social and cultural features may make a difference to a life lived with schizophrenia. And if we understand culture’s impact more deeply, we believe that we may improve the way we reach out to help those who struggle with our most troubling madness.

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