Housing familiar male wildtype rats together reduces the long-term adverse behavioural and physiological effects of social defeat

1999 ◽  
Vol 24 (3) ◽  
pp. 285-300 ◽  
Author(s):  
M.A.W Ruis ◽  
J.H.A te Brake ◽  
B Buwalda ◽  
S.F De Boer ◽  
P Meerlo ◽  
...  
Keyword(s):  
Social Defeat ◽  
Physiological Effects

scholarly journals Stress vulnerability promotes an alcohol prone phenotype in a preclinical model of sustained depression

2018 ◽  
Author(s):  
Danai Riga ◽  
Leanne JM Schmitz ◽  
Yvar van Mourik ◽  
Witte JG Hoogendijk ◽  
Taco J De Vries ◽  
...  
Keyword(s):  
Social Defeat ◽  
Preclinical Model ◽  
Self Administration ◽  
Depression Vulnerability ◽  
Stress Vulnerability ◽  
The Social ◽  
Depression Proneness ◽  
Male Wistar Rats ◽  
Alcohol Seeking

AbstractMajor depression and alcohol-related disorders frequently co-occur. Depression severity weighs on the magnitude and persistence of comorbid alcohol use disorder (AUD), with severe implications for disease prognosis. Here, we investigated whether depression vulnerability drives propensity to AUD at the preclinical level. We used the social defeat-induced persistent stress (SDPS) model of chronic depression in combination with operant alcohol self-administration (SA). Male Wistar rats were subjected to social defeat (5 episodes) and prolonged social isolation (~12 weeks) and subsequently classified as SDPS-prone or SDPS-resilient based on their affective and cognitive performance. Using an operant alcohol SA paradigm, acquisition, motivation, extinction and cue-induced reinstatement of alcohol-seeking were examined in the two subpopulations. SDPS-prone animals showed increased alcohol SA, excessive motivation to acquire alcohol, persistent alcohol-seeking despite alcohol unavailability, extinction resistance and increased cue-induced relapse; the latter could be blocked by the α2 adrenoreceptor agonist guanfacine. In SDPS-resilient rats, prior exposure to social defeat increased alcohol SA without affecting any other measures of alcohol-seeking and -taking. Our data revealed that depression proneness confers vulnerability to alcohol, emulating patterns of alcohol dependence seen in human addicts, and that depression resilience to a large extent protects from the development of AUD-like phenotypes. Furthermore, our data suggest that stress exposure alone, independently of depressive symptoms, alters alcohol intake in the long-term.

scholarly journals Intentional replacement of dead children in sub-Saharan Africa: evidence from Ghana and Kenya

2004 ◽  
Vol 31 (1) ◽  
pp. 33 ◽  
Author(s):  
Stephen Obeng Gyimah ◽  
Rajulton Fernando
Keyword(s):  
Childhood Mortality ◽  
Policy Implications ◽  
Sub Saharan Africa ◽  
Physiological Effects ◽  
Short Term ◽  
Mortality Experience ◽  
First Child ◽  
Health Survey Data ◽  
Sub Saharan

This paper examines whether childhood deaths elicit an explicit, conscious and intentional fertility response using the 1998 Demographic and Health Survey data for Ghana and Kenya . Using multivariate hazard models, childhood mortality experience was found to have long term fertility implications beyond the short term physiological effects. In both countries, women who have experienced childhood mortality were found to have significantly higher number of additional children than those without. The death of the first child in particular was found to be associated with the risk of a higher order birth consistent with recent findings in Cameroon. The policy implications of the findings are discussed.

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.

scholarly journals Repeated social defeat induces transient glial activation and brain hypometabolism: A positron emission tomography imaging study

2017 ◽  
Vol 39 (3) ◽  
pp. 439-453 ◽  
Author(s):  
Paula Kopschina Feltes ◽  
Erik FJ de Vries ◽  
Luis E Juarez-Orozco ◽  
Ewelina Kurtys ◽  
Rudi AJO Dierckx ◽  
...  
Keyword(s):  
Positron Emission Tomography ◽  
Positron Emission Tomography Imaging ◽  
Imaging Study ◽  
Social Defeat ◽  
Glial Activation ◽  
Emission Tomography ◽  
Biochemical Alterations ◽  
Positron Emission

Psychosocial stress is a risk factor for the development of depression. Recent evidence suggests that glial activation could contribute to the development of depressive-like behaviour. This study aimed to evaluate in vivo whether repeated social defeat (RSD) induces short- and long-term inflammatory and metabolic alterations in the brain through positron emission tomography (PET). Male Wistar rats ( n = 40) were exposed to RSD by dominant Long-Evans rats on five consecutive days. Behavioural and biochemical alterations were assessed at baseline, day 5/6 and day 24/25 after the RSD protocol. Glial activation (11C-PK11195 PET) and changes in brain metabolism (18F-FDG PET) were evaluated on day 6, 11 and 25 (short-term), and at 3 and 6 months (long-term). Defeated rats showed transient depressive- and anxiety-like behaviour, increased corticosterone and brain IL-1β levels, as well as glial activation and brain hypometabolism in the first month after RSD. During the third- and six-month follow-up, no between-group differences in any investigated parameter were found. Therefore, non-invasive PET imaging demonstrated that RSD induces transient glial activation and reduces brain glucose metabolism in rats. These imaging findings were associated with stress-induced behavioural changes and support the hypothesis that neuroinflammation could be a contributing factor in the development of depression.

scholarly journals The high-altitude research of Mabel Purefoy FitzGerald, 1911–13

2014 ◽  
Vol 69 (1) ◽  
pp. 85-99
Author(s):  
Martin Goodman
Keyword(s):  
Science Education ◽  
High Altitude ◽  
Physiological Effects ◽  
Alveolar Air ◽  
Team Members ◽  
Mining Communities ◽  
Colorado Rockies ◽  
Home Schooled

Home schooled without a science education, Mabel Purefoy FitzGerald (1872–1973) attended physiology lectures at Oxford in 1897, even though the school was closed to women. She found work as a researcher, published early noted papers and earned the active respect and support of senior scientists of her day. Her laboratory work with the physiologist J. S. Haldane saw her invited to the join the Pikes Peak Expedition in 1911. While the male team members measured the physiological effects of long-term residency at 14 101 feet, as the sole woman FitzGerald took measurements of haemoglobin and alveolar air from herself and from mining staff and families at altitudes from 6000 to 12 500 feet, travelling to remote mining communities in the Colorado Rockies. A subsequent expedition collected data at lower altitudes. Recorded in two papers, the results presented pioneering evidence of the role of oxygen in breathing.

scholarly journals Social defeat: Risk factor for schizophrenia?

2005 ◽  
Vol 187 (2) ◽  
pp. 101-102 ◽  
Author(s):  
Jean-Paul Selten ◽  
Elizabeth Cantor-Graae
Keyword(s):  
Risk Factor ◽  
Social Defeat ◽  
Dopamine System ◽  
Mesolimbic Dopamine System ◽  
Baseline Activity ◽  
Increased Risk ◽  
The Social ◽  
System Data ◽  
Long Term Experience

SummaryThe hypothesis that chronic and long-term experience of ‘social defeat’ may increase the risk for schizophrenia is proposed. This increased risk may result from sensitisation of the mesolimbic dopamine system and/or increased baseline activity of this system. Data supporting the social defeat hypothesis are presented.

scholarly journals Heart Rate Variability Time Analyses of the Streptozotocin- Diabetic Rat

2007 ◽  
Vol 4 (1) ◽  
pp. 64
Author(s):  
M. Jacobson ◽  
F.C. Howarth ◽  
E. Adeghate ◽  
K. Fatima-Shad
Keyword(s):  
Heart Rate ◽  
Heart Rate Variability ◽  
Diabetic Rat ◽  
Physiological Effects ◽  
Short Term ◽  
The World ◽  
Electrocardiogram Ecg ◽  
Prevalence Of Diabetes Mellitus ◽  
Streptozotocin Diabetic Rat

As the world prevalence of diabetes mellitus (DM) increases, animal models of the disease's progression are required for researching effective treatment. The streptozotocin (STZ) treated rat is known to cause hyperglycaemia. This study confirms that this animal model also displays DM physiological effects in the animal heart rate (HR) and heart rate variability (HRV). In particular, 5 minutes of rat (n=13) electrocardiogram (ECG) is acquired hourly for 30 days. At day 10, the animal (n=7) is dosed with STZ and the ECG is analyzed in order to determine the HR and HRV. The HRV is indexed using two time-based analyses, based on long-term (24hr) and short-term (5min) analyses. All analyses are compared to control non-STZ dosed animals (n=6) and display significant DM effects. 

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