Learned immobility explains the behavior of rats in the forced swimming test

Pablo, J; Parra, Andrés; Segovia, Santiago; Guillamón, Antonio

doi:10.1016/0031-9384(89)90261-8

Cited by 156 publications

(95 citation statements)

References 54 publications

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“…This paradigm offers important advantages over other models of depression: first, it induces in rodents an array of abnormal behaviors that are isomorphic with key features of human depression (Willner 2005); second, CMS-exposed rats-like depressed patients-respond to chronic, but not acute, treatment with antidepressant drugs (Willner 1997); third, psychostimulant agents, which can give false positives in acute stress-based models (De Pablo et al 1989;Duncan et al 1985;Steru et al 1985), have no such effects in CMS . The present results show that BW gain and sucrose intake are significantly reduced by CMS and are corrected by chronic treatment with URB597.…”

Section: Discussionmentioning

confidence: 99%

Antidepressant-like Activity of the Fatty Acid Amide Hydrolase Inhibitor URB597 in a Rat Model of Chronic Mild Stress

Bortolato

Mangieri

et al. 2007

Biological Psychiatry

311

252

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Section: Discussionmentioning

confidence: 99%

Antidepressant-like Activity of the Fatty Acid Amide Hydrolase Inhibitor URB597 in a Rat Model of Chronic Mild Stress

Bortolato

Mangieri

et al. 2007

Biological Psychiatry

311

252

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show abstract

“…Well-known learning and memory paradigms include the Morris water maze, the radial maze and the forced swim test. In these tests the animal learns to choose the most appropriate behavioral response to enhance the chance of survival (finding the platform in the Morris water maze; 1 conservation of energy by floating in the forced swim test [2][3][4][5] ) and reward (food in the radial maze). As these and most other behavioral tests involve aversive and anxiogenic conditions (e.g., novelty, fear, sleep deprivation), stress hormones such as glucocorticoid hormones (corticosterone in rats and mice) are secreted during the learning sessions.…”

Section: Introductionmentioning

confidence: 99%

Epigenetic mechanisms in the dentate gyrus act as a molecular switch in hippocampus-associated memory formation

Reul¹,

Hesketh²,

Collins³

et al. 2009

Epigenetics

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We make strong memories of significant events in our lives which may serve to increase our resilience and adaptation capacity to deal with future challenges. It is well established that the neurotransmitter glutamate and the ERK MAPK intracellular signaling pathway play a principal role in memory formation. In addition, stressassociated hormones like glucocorticoids released during such events are known to strengthen formation of memories. But, how do these hormones work? Do they interact with the ERK MAPK pathway or otherwise? What are the more distal, epigenomic effects? We discovered in rats and mice that confrontation with a psychological challenge (e.g., forced swimming, Morris water maze) would lead, through NMDA-ERK signaling, to MSK1 and Elk-1 activation in dentate gyrus neurons (a part of the hippocampus involved in encoding of memories) resulting in histone H3 S10-phosphorylation and K14-acetylation, H4 hyper-acetylation, gene induction and formation of memories of the event. Moreover, glucocorticoid hormones via the glucocorticoid receptor (GR) greatly facilitated the epigenomic mechanisms and cognitive performance. Therefore, we propose that formation of enduring memories of significant events requires an interaction of GRs with the NMDA/ ERK/MSK1/Elk-1 signaling pathways to allow an optimal epigenomic activation pattern in dentate gyrus neurons to accommodate their altered neurophysiological function.

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“…Some authors have argued that immobility is largely dependent on learning and memory. 291,292 However, most of the bases for such hypotheses are centered on the two-test rat model and hence are largely redundant in the mouse version of the test. Nonetheless, there has been very little research focused on the role of cognitive process in the mouse FST; however, it should be noted that the muscarinic antagonist and amnesiac scopolamine prevents the induction of immobility in the test.…”

Section: Widely Used Murine Models Of Depressionmentioning

confidence: 99%

In search of a depressed mouse: utility of models for studying depression-related behavior in genetically modified mice

2004

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The ability to modify mice genetically has been one of the major breakthroughs in modern medical science affecting every discipline including psychiatry. It is hoped that the application of such technologies will result in the identification of novel targets for the treatment of diseases such as depression and to gain a better understanding of the molecular pathophysiological mechanisms that are regulated by current clinically effective antidepressant medications. The advent of these tools has resulted in the need to adopt, refine and develop mouse-specific models for analyses of depression-like behavior or behavioral patterns modulated by antidepressants. In this review, we will focus on the utility of current models (eg forced swim test, tail suspension test, olfactory bulbectomy, learned helplessness, chronic mild stress, drug-withdrawal-induced anhedonia) and research strategies aimed at investigating novel targets relevant to depression in the mouse. We will focus on key questions that are considered relevant for examining the utility of such models. Further, we describe other avenues of research that may give clues as to whether indeed a genetically modified animal has alterations relevant to clinical depression. We suggest that it is prudent and most appropriate to use convergent tests that draw on different antidepressant-related endophenotypes, and complimentary physiological analyses in order to provide a program of information concerning whether a given phenotype is functionally relevant to depressionrelated pathology.

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Learned immobility explains the behavior of rats in the forced swimming test

Cited by 156 publications

References 54 publications

Antidepressant-like Activity of the Fatty Acid Amide Hydrolase Inhibitor URB597 in a Rat Model of Chronic Mild Stress

Antidepressant-like Activity of the Fatty Acid Amide Hydrolase Inhibitor URB597 in a Rat Model of Chronic Mild Stress

Epigenetic mechanisms in the dentate gyrus act as a molecular switch in hippocampus-associated memory formation

In search of a depressed mouse: utility of models for studying depression-related behavior in genetically modified mice

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