Immobility behavior during the forced swim test correlates with BNDF levels in the frontal cortex, but not with cognitive impairments

Borsoi, Milene; Antonio, Camila B.; Viana, Alice Fialho; Nardin, Patrícia; Gonçalves, Carlos-Alberto; Rates, Stela Maris Kuze

doi:10.1016/j.physbeh.2014.12.024

Cited by 29 publications

(14 citation statements)

References 67 publications

(86 reference statements)

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“…Immobility time during FS is a behavioral measure of despair . Our previous study showed that the 3 day FS paradigm significantly increased the immobility time .…”

Section: Resultsmentioning

confidence: 99%

“…Immobility time during FS is a behavioral measure of despair. 31 Our previous study showed that the 3 day FS paradigm significantly increased the immobility time. 18 Here we found that the immobility time significantly increased following bilateral masseter injection with CFA or saline followed by FS in E2 or oil-treated OVx rats (Two-way ANOVA, day effect, F 2,132 =5.820, P=.004; group effect, F 2,132 =19.37, P<.0001; interaction effect, F 4,132 =0.2033, P=.936).…”

Section: Repeated Fs With Craniofacial Inflammation Induced Depressmentioning

confidence: 93%

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Extracellular signal‐regulated kinase activation in the spinal cord contributes to visceral hypersensitivity induced by craniofacial injury followed by stress

Zhao

et al. 2017

Neurogastroenterology Motil

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“…Immobility time during FS is a behavioral measure of despair . Our previous study showed that the 3 day FS paradigm significantly increased the immobility time .…”

Section: Resultsmentioning

confidence: 99%

Section: Repeated Fs With Craniofacial Inflammation Induced Depressmentioning

confidence: 93%

Extracellular signal‐regulated kinase activation in the spinal cord contributes to visceral hypersensitivity induced by craniofacial injury followed by stress

Zhao

et al. 2017

Neurogastroenterology Motil

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“…The BDNF protein is involved in neuroprotective effect and serves as an essential signaling molecule to recovery brain injury in some severe cerebral diseases. BDNF functions as the important modulator in stress‐induced LTP in hippocampus (Fanaei et al, ; Borsoi et al, ). Trkb is a high‐affinity receptor and function modulator for BDNF.…”

Section: Discussionmentioning

confidence: 99%

Involvement of mTOR‐related signaling in antidepressant effects of Sophoraflavanone G on chronically stressed mice

Wang

Tong

Xiao

et al. 2020

Phytotherapy Research

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SophoraflavanoneG (SG), an important prenylated flavonoid isolated from Sophoraalopecuroides.L, is effective for many illnesses. The present study was designed to investigate whether the compound could reverse depressive‐like symptoms and investigate its possible mechanisms. Chronic Unpredictable Mild Stress (CUMS) mice were treated with fluoxetine and SG. The immobility time in forced swimming test (FST) and tail suspension test (TST) were recorded. The levels of pro‐inflammatory cytokines and neurotransmitters in the hippocampus were evaluated. Furthermore, the protein expressions of PI3K, AKT, mTOR, p70S6K, BDNF, and Trkb in hippocampus were detected. Rapamycin, the selective mTOR inhibitor, was used to estimate the potential mechanism. As a result, after 7 days of SG treatment, the immobility time in FST and TST was declined obviously. The levels of IL‐6, IL‐1β, and TNF‐α in the hippocampus were significantly reduced, and the quantity of 5‐HT and NE was raised considerably in SG‐treated group compared with the CUMS‐exposed group. Additionally, SG could up‐regulate the expressions of PI3K, AKT, mTOR, 70S6K, BDNF, and Trkb. The blockade of mammalian target of rapamycin signaling blunted the antidepressant effect and reversed the up‐regulation of BDNF expression caused by SG. These findings suggested that SG treatment alleviated depressive‐like symptoms via mTOR‐mediated BDNF/Trkb signaling.

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“…It has been proposed that after repeated swimming animals learn that move is useless and become immobile faster and for a longer period for saving energy (Borsini et al 1986, de Kloet and Molendijk 2016, Masuda et al 2001, Parra et al 1999, West 1990. However, studies showing a deleterious effect of the repeated forced swim on cognitive tasks, such as the Morris water maze (Abel and Hannigan 1992, Rates 1998), novel object recognition (Yuen et al 2012), object location (Borsoi et al 2015a) and prepulse inhibition tests (Borsoi et al 2015a, b), contradict this successful strategy theory. On the other hand, immobility behavior in the forced swimming has been also related to schizophrenia negative symptoms, as apathy and lack of initiative (Langen et al 2012, Noda et al 1995, Porsolt et al 2010).…”

Section: Introductionmentioning

confidence: 99%

“…Locomotion in response to novelty and novel object recognition (tasks related to positive and cognitive impairments presented by schizophrenia patients, respectively) were also performed in order to make a broader evaluation. The methodology used was based on that described by Noda et al (1995Noda et al ( , 1997 with some modifications according to the standard protocol used by our group (Viana et al 2008, Borsoi et al 2015a. Animals were habituated to laboratory conditions one hour before exposition to the forced swimming session.…”

Section: Introductionmentioning

confidence: 99%

Is Forced Swimming Immobility a Good Endpoint for Modeling Negative Symptoms of Schizophrenia? - Study of Sub-Anesthetic Ketamine Repeated Administration Effects

Neves

Borsoi

Antonio

et al. 2017

An. Acad. Bras. Ciênc.

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Immobility time in the forced swimming has been described as analogous to emotional blunting or apathy and has been used for characterizing schizophrenia animal models. Several clinical studies support the use of NMDA receptor antagonists to model schizophrenia in rodents. Some works describe the effects of ketamine on immobility behavior but there is variability in the experimental design used leading to controversial results. In this study, we evaluated the effects of repeated administration of ketamine subanesthetic doses in forced swimming, locomotion in response to novelty and novel object recognition, aiming a broader evaluation of the usefulness of this experimental approach for modeling schizophrenia in mice. Ketamine (30 mg/kg/day i.p. for 14 days) induced a not persistent decrease in immobility time, detected 24h but not 72h after treatment. This same administration protocol induced a deficit in novel object recognition. No change was observed in mice locomotion. Our results confirm that repeated administration of sub-anesthetic doses of ketamine is useful in modeling schizophrenia-related behavioral changes in mice. However, the immobility time during forced swimming does not seem to be a good endpoint to evaluate the modeling of negative symptoms in NMDAR antagonist animal models of schizophrenia.

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Immobility behavior during the forced swim test correlates with BNDF levels in the frontal cortex, but not with cognitive impairments

Cited by 29 publications

References 67 publications

Extracellular signal‐regulated kinase activation in the spinal cord contributes to visceral hypersensitivity induced by craniofacial injury followed by stress

Extracellular signal‐regulated kinase activation in the spinal cord contributes to visceral hypersensitivity induced by craniofacial injury followed by stress

Involvement of mTOR‐related signaling in antidepressant effects of Sophoraflavanone G on chronically stressed mice

Is Forced Swimming Immobility a Good Endpoint for Modeling Negative Symptoms of Schizophrenia? - Study of Sub-Anesthetic Ketamine Repeated Administration Effects

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