Neurobehavioral studies of forced swimming: The role of learning and memory in the forced swim test

West, Aprilia

doi:10.1016/0278-5846(90)90073-p

Cited by 211 publications

(122 citation statements)

References 30 publications

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“…The increase in baseline immobility exhibited by GRov mice is indicative of a substantial depressant-like effect of the genetic manipulation. Alternative explanations involving learning capability and an energy conserving strategy remain a possibility (22). A notable finding of the present study is that the increase in GR expression in the forebrain leads to an increased response sensitivity to antidepressants in FST, including tricyclic antidepressants and a selective serotonin reuptake inhibitor (Fig.…”

Section: Discussionmentioning

confidence: 67%

Glucocorticoid receptor overexpression in forebrain: A mouse model of increased emotional lability

Wei

Lü

Liu

et al. 2004

Proc. Natl. Acad. Sci. U.S.A.

229

164

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The molecular mechanisms that control the range and stability of emotions are unknown, yet this knowledge is critical for understanding mood disorders, especially bipolar illness. Here, we show that the glucocorticoid receptor (GR) modulates these features of emotional responsiveness. We generated transgenic mice overexpressing GR specifically in forebrain. These mice display a significant increase in anxiety-like and depressant-like behaviors relative to wild type. Yet, they are also supersensitive to antidepressants and show enhanced sensitization to cocaine. Thus, mice overexpressing GR in forebrain have a consistently wider than normal range of reactivity in both positive and negative emotionality tests. This phenotype is associated, in specific brain regions, with increased expression of genes relevant to emotionality: corticotropin-releasing hormone, serotonin, norepinephrine and dopamine transporters, and 5-hydroxytryptamine 1A receptor. Thus, GR overexpression in forebrain causes higher ''emotional lability'' secondary to a unique pattern of molecular regulation. This finding suggests that natural variations in GR gene expression can contribute to the fine-tuning of emotional stability or lability and may play a role in bipolar disorder.

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Section: Discussionmentioning

confidence: 67%

Glucocorticoid receptor overexpression in forebrain: A mouse model of increased emotional lability

Wei

Lü

Liu

et al. 2004

Proc. Natl. Acad. Sci. U.S.A.

229

164

View full text Add to dashboard Cite

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“…This phenotype was most prominent during the first exposure (day 1; Figure 1) and vanished towards the third exposure (day 21), likely because of interplay between stress-coping and long-term memory. 47 These findings of increased floating, especially on day 1, were substantiated by the pharmacological blockade of CB1 receptors in C57BL/6N mice ( Figure 2) and in CB1 þ / þ mice ( Figure 3). Thus, our behavioral data imply that the blockade of CB1 receptors in mice leads to depressive-like symptoms in the FST.…”

Section: Discussionmentioning

confidence: 82%

Impaired cannabinoid receptor type 1 signaling interferes with stress-coping behavior in mice

et al. 2007

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Dysregulation of the endocannabinoid system is known to interfere with emotional processing of stressful events. Here, we studied the role of cannabinoid receptor type 1 (CB1) signaling in stress-coping behaviors using the forced swim test (FST) with repeated exposures. We compared effects of genetic inactivation with pharmacological blockade of CB1 receptors both in male and female mice. In addition, we investigated potential interactions of the endocannabinoid system with monoaminergic and neurotrophin systems of the brain. Naive CB1 receptor-deficient mice (CB1 À/À ) showed increased passive stress-coping behaviors as compared to wild-type littermates (CB1 þ / þ ) in the FST, independent of sex. These findings were partially reproduced in C57BL/6N animals and fully reproduced in female CB1 þ / þ mice by pharmacological blockade of CB1 receptors with the CB1 receptor antagonist SR141716. The specificity of SR141716 was confirmed in female CB1 À/À mice, where it failed to affect behavioral performance. Sensitivity to the antidepressants desipramine and paroxetine was preserved, but slightly altered in female CB1 À/À mice. There were no genotype differences between CB1 þ / þ and CB1 À/À mice in monoamine oxidase A and B activities under basal conditions, nor in monoamine content of hippocampal tissue after FST exposure. mRNA expression of vesicular glutamate transporter type 1 was unaffected in CB1 À/À mice, but mRNA expression of brain-derived neurotrophic factor (BDNF) was reduced in the hippocampus. Our results suggest that impaired CB1 receptor function promotes passive stress-coping behavior, which, at least in part, might relate to alterations in BDNF function.

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“…(3) The time spent in inactive posture (immobility) depends also on the subject`s temperament and coping style. The well-known depression test, forced swimming measures also the coping of the animals, however some authors suggested that it reflected effects of learning and memory rather than effects of despair or depression [65]. According to these assumptions the diminished immobility time of AVP-deficient rats during the forced swimming test [37] could be interpreted as changes in temperament [8,26], more active coping style or even learning disabilities.…”

Section: Discussionmentioning

confidence: 99%

Increase in Alzheimer's related markers preceeds memory disturbances: Studies in vasopressin-deficient Brattleboro rat

Várga

Klausz

Domokos

et al. 2014

Brain Research Bulletin

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Alzheimer's disease (AD) is the most common form of dementia in the elderly. For more effective therapy early diagnostic markers could be beneficial. Therefore we compared one year old rats with adults and examined if changes in possible brain markers of AD preceeded memory decline. We also tested if vasopressin-deficient animals were useful model of AD as vasopressin has well known positive effect on memory and AD patient has decreased vasopressin production.We compared adult (3 month) and old (12 month), normal and vasopressin-deficient Brattleboro rats. To receive a comprehensive picture about their memory we examined their social discrimination, object discrimination and conditioned learning abilities (shuttle box).Amyloid precursor protein (APP), mitogen-activated protein kinase 1 (MAPK1), β-actin and tryptophan 2,3-dioxygenase 2 (TDO2) mRNA levels was measured by quantitative PCR.There was no difference between the memory of adult and aged groups. The vasopressin-deficient rats at both ages showed a weaker performance in the course of social and object discrimination tests and a higher escape failure during the shuttle box experiment. The brain marker mRNAs of the elder animals were higher than the levels of the adults, but the absence of vasopressin had no influence on them.Thus, the one year old rats showed elevated levels of AD-related markers, but memory deficits were observable only in vasopressin deficient animals. Vasopressin does not seem to have pathogenic role in AD. Changes in the studied markers might predict later symptoms, although further studies are required for confirmation.

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Neurobehavioral studies of forced swimming: The role of learning and memory in the forced swim test

Cited by 211 publications

References 30 publications

Glucocorticoid receptor overexpression in forebrain: A mouse model of increased emotional lability

Glucocorticoid receptor overexpression in forebrain: A mouse model of increased emotional lability

Impaired cannabinoid receptor type 1 signaling interferes with stress-coping behavior in mice

Increase in Alzheimer's related markers preceeds memory disturbances: Studies in vasopressin-deficient Brattleboro rat

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