Antidepressant-like effects in various mice strains in the forced swimming test

David, Denis J.; Renard, Caroline; Jolliet, Pascale; Hascoët, Martine; Bourin, Michel

doi:10.1007/s00213-002-1335-4

Cited by 165 publications

(120 citation statements)

References 37 publications

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“…Some authors have postulated that it is the high brain dopamine level in this strain that is a limiting factor for the antidepressant-like effects of ADs in this test (Renard et al, 2004). However, in our hands, WT animals were responsive to the acute and repeated administration of the antidepressants used in the present study, with the exception of citalopram, which was not effective, similar as in the studies reported by David et al (2003).…”

Section: Discussionsupporting

confidence: 87%

“…The strain of mice strongly influences the animal response in the FST (Alcaro et al, 2002;David et al, 2003;Lucki et al, 2001), with C57BL/6J mice being moderately responsive to ADs in this test. Some authors have postulated that it is the high brain dopamine level in this strain that is a limiting factor for the antidepressant-like effects of ADs in this test (Renard et al, 2004).…”

Section: Discussionmentioning

confidence: 98%

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Effect of Antidepressant Drugs in Mice Lacking the Norepinephrine Transporter

Dziedzicka-Wasylewska

Faron-Górecka

Kuśmider

et al. 2006

Neuropsychopharmacol

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One of the main theories concerning the mechanism of action of antidepressant drugs (ADs) is based on the notion that the neurochemical background of depression involves an impairment of central noradrenergic transmission with a concomitant decrease of the norepinephrine (NE) in the synaptic gap. Many ADs increase synaptic NE availability by inhibition of the reuptake of NE. Using mice lacking NE transporter (NET À/À ) we examined their baseline phenotype as well as the response in the forced swim test (FST) and in the tail suspension test (TST) upon treatment with ADs that display different pharmacological profiles. In both tests, the NET À/À mice behaved like wild-type (WT) mice acutely treated with ADs. Autoradiographic studies showed decreased binding of the b-adrenergic ligand [ 3 H]CGP12177 in the cerebral cortex of NET À/À mice, indicating the changes at the level of b-adrenergic receptors similar to those obtained with ADs treatment. The binding of [ 3 H]prazosin to a 1 -adrenergic receptors in the cerebral cortex of NET À/À mice was also decreased, most probably as an adaptive response to the sustained elevation of extracellular NE levels observed in these mice. A pronounced NET knockout-induced shortening of the immobility time in the TST (by ca 50%) compared to WT mice was not reduced any further by NET-inhibiting ADs such as reboxetine, desipramine, and imipramine. Citalopram, which is devoid of affinity for the NET, exerted a significant reduction of immobility time in the NET À/À mice. In the FST, reboxetine, desipramine, imipramine, and citalopram administered acutely did not reduce any further the immobility time shortened by NET knockout itself (ca 25%); however, antidepressant-like action of repeatedly (7 days) administered desipramine was observed in NET À/À mice, indicating that the chronic presence of this drug may also affect other neurochemical targets involved in the behavioral reactions monitored by this test. From the present study, it may be concluded that mice lacking the NET may represent a good model of some aspects of depression-resistant behavior, paralleled with alterations in the expression of adrenergic receptors, which result as an adaptation to elevated levels of extracellular NE.

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Section: Discussionsupporting

confidence: 87%

Section: Discussionmentioning

confidence: 98%

Effect of Antidepressant Drugs in Mice Lacking the Norepinephrine Transporter

Dziedzicka-Wasylewska

Faron-Górecka

Kuśmider

et al. 2006

Neuropsychopharmacol

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“…Ambiguous results concerning the sensitivity of DBA/2 mice towards the effects of antidepressants were reported. Some studies found the DBA/2 strain to be antidepressant-sensitive (Lucki et al 2001;Crowley et al 2005), whereas others did not (David et al 2003;Cervo et al 2005). The underlying reasons for this discrepancy still remain to be determined.…”

Section: Slc25a18mentioning

confidence: 95%

“…The FST and testing in the dark/light box were performed 4 h after last application in order to confirm the behavioral effects of the treatment at the same time point when the brains of test-naïve-treated mice were taken for microarray analysis. The mHB was performed 30 min after last application as many published results on behavioral effects of antidepressants were assessed at this time point (e.g., Lucki et al 2001;David et al 2003;Crowley et al 2005).…”

Section: Behavioral Testingmentioning

confidence: 99%

Profiling of behavioral changes and hippocampal gene expression in mice chronically treated with the SSRI paroxetine

et al. 2008

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Introduction Monoamine-based antidepressants inhibit neurotransmitter reuptake within short time. However, it commonly takes several weeks until clinical symptoms start to resolve-indicating the involvement of effects distant from reuptake inhibition. Objective To unravel other mechanisms involved in drug action, a "reverse" pharmacological approach was applied to determine antidepressant-induced alterations of hippocampal gene expression. Materials and methodsThe behavioral response to longterm paroxetine administration of male DBA/2Ola mice was assessed by the forced swim test (FST), the modified hole board (mHB), and the dark/light box. Hippocampi of test-naive mice were dissected, and changes in gene expression by paroxetine treatment were investigated by means of microarray technology. Results and discussion Robust effects of paroxetine on passive stress-coping behavior in the FST were observed. Furthermore, anxiolytic properties of long-term antidepressant treatment could be identified in DBA mice in both, the mHB and dark/light box. Analysis of microarray results revealed a list of 60 genes differentially regulated by chronic paroxetine treatment. Preproenkephalin 1 and inhibin beta-A showed the highest level of transcriptional change. Furthermore, a number of candidates involved in neuroplasticity/neurogenesis emerged (e.g., Bdnf, Gfap, Vim, Sox11, Egr1, Stat3). Seven selected candidates were confirmed by in situ hybridization. Additional immunofluorescence colocalization studies of GFAP and vimentin showed more positive cells to be detected in long-term paroxetine-treated DBA mice. Conclusion Candidate genes identified in the current study using a mouse strain validated for its responsiveness to long-term paroxetine treatment add, in our opinion, to unraveling the mechanism of action of paroxetine as a representative for SSRIs.

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“…The forced swimming test was performed according to the method described previously [22] . Mice were put singly into transparent Plexiglas cylinders (height: 24 cm, diameter: 13 cm) containing water at a depth of 10 cm, maintained at 22 °C for 6 min.…”

Section: Forced Swimming Test (Fst)mentioning

confidence: 99%

Novel κ-opioid receptor agonist MB-1C-OH produces potent analgesia with less depression and sedation

et al. 2015

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Aim: To characterize the pharmacological profiles of a novel κ-opioid receptor agonist MB-1C-OH. Methods: [ 3 H]diprenorphine binding and [ 35 S]GTPγS binding assays were performed to determine the agonistic properties of MB-1C-OH. Hot plate, tail flick, acetic acid-induced writhing, and formalin tests were conducted in mice to evaluate the antinociceptive actions. Forced swimming and rotarod tests of mice were used to assess the sedation and depression actions. Results: In [ 3 H]diprenorphine binding assay, MB-1C-OH did not bind to μ-and δ-opioid receptors at the concentration of 100 μmol/L, but showed a high affinity for κ-opioid receptor (K i =35 nmol/L). In [ 35 S]GTPγS binding assay, the compound had an E max of 98% and an EC 50 of 16.7 nmol/L for κ-opioid receptor. Subcutaneous injection of MB-1C-OH had no effects in both hot plate and tail flick tests, but produced potent antinociception in the acetic acid-induced writhing test (ED 50 =0.39 mg/kg), which was antagonized by pretreatment with a selective κ-opioid receptor antagonist Nor-BNI. In the formalin test, subcutaneous injection of MB-1C-OH did not affect the flinching behavior in the first phase, but significantly inhibited that in the second phase (ED 50 =0.87 mg/kg). In addition, the sedation or depression actions of MB-1C-OH were about 3-fold weaker than those of the classical κ agonist (-)U50,488H. Conclusion: MB-1C-OH is a novel κ-opioid receptor agonist that produces potent antinociception causing less sedation and depression.

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Antidepressant-like effects in various mice strains in the forced swimming test

Cited by 165 publications

References 37 publications

Effect of Antidepressant Drugs in Mice Lacking the Norepinephrine Transporter

Effect of Antidepressant Drugs in Mice Lacking the Norepinephrine Transporter

Profiling of behavioral changes and hippocampal gene expression in mice chronically treated with the SSRI paroxetine

Novel κ-opioid receptor agonist MB-1C-OH produces potent analgesia with less depression and sedation

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