Repeated social defeat or repeated ethanol: Consequences on ethanol drinking and ethanol-induced psychomotor effects in mice

Alcohol ◽  
2017 ◽  
Vol 60 ◽  
pp. 239
Author(s):  
G.C. Macedo ◽  
D. Suchecki ◽  
I.M.H. Quadros
Keyword(s):  
Social Defeat ◽  
Psychomotor Effects ◽  
Ethanol Drinking

scholarly journals Consequence of Two Protocols of Social Defeat Stress on Nicotine-Induced Psychomotor Effects in Mice

2019 ◽  
Vol 2019 ◽  
pp. 1-12
Author(s):  
Liz Paola Domingues ◽  
Bruno de Brito Antonio ◽  
Maria Gabriela Menezes de Oliveira ◽  
Isabel Marian Hartmann de Quadros
Keyword(s):  
Social Defeat ◽  
Acute Administration ◽  
Locomotor Response ◽  
Social Defeat Stress ◽  
Psychomotor Effects ◽  
Locomotor Stimulation ◽  
Nicotine Administration ◽  
Drug Use Disorders ◽  
Dose Dependent

Exposure to stress may contribute to enhanced vulnerability to drug use disorders, by altering sensitivity to drug-related reward and psychomotor effects. This study aimed to characterize the psychomotor effects of nicotine administration and then investigate the consequences of two types of repeated social defeat stress (episodic and continuous) on nicotine-induced psychomotor effects in mice. Adult male Swiss mice were treated for 13 days with daily injections of nicotine (0.1, 0.4, or 1.0 mg/kg, s.c.) and received saline and nicotine challenges (0, 0.1 and 0.4 mg/kg) after a withdrawal period. Dose-dependent effects were observed in locomotor response to nicotine, with trends for locomotor stimulation after intermittent (but not acute) administration of 0.1 mg/kg. Higher nicotine doses caused acute locomotor suppression (0.4 and 1.0 mg/kg) and tolerance after intermittent administration (0.4 mg/kg dose). In separate cohorts, experimental mice were daily defeated by aggressive mice, using the resident-intruder model, for 10 days. After brief confrontations, intruders returned to their home cage (episodic stress) or were continuously exposed to the aggressive resident for 24 h (continuous stress), until the following defeat. After the 10-day stress protocol, mice received saline and nicotine challenges (0 and 0.1 mg/kg, s.c.) in locomotor tests. Mice were also tested for methamphetamine-induced locomotor response (1.0 mg/kg, i.p.). Both defeat protocols induced short-term locomotor suppression (24h after stress), which was further suppressed by nicotine only in mice exposed to continuous defeat stress. Ten days after stress, locomotor behavior was no longer suppressed in defeated mice of either stress protocol. Mice exposed to continuous defeat stress showed a reduced stimulant response to methamphetamine, 12 days after termination of stress. Our findings indicate that exposure to continuous defeat stress facilitates nicotine-induced locomotor suppression shortly after stress and reduces methamphetamine-induced stimulation in the long term.

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

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

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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