In the rat forced swimming test, chronic but not subacute administration of dual 5-HT/NA antidepressant treatments may produce greater effects than selective drugs

Rénéric, Jean-Philippe; Bouvard, Manuel; Stinus, Luis

doi:10.1016/s0166-4328(02)00203-6

Cited by 71 publications

(43 citation statements)

References 53 publications

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“…Temporal specificity of antidepressant behavioral effects in the FST have also been reported in C57Bl/6 mice treated with chronic amitriptyline (21 days, via drinking water) (Caldarone et al, 2003), and in rats treated with fluoxetine via osmotic minipumps (Cryan et al, 2005). However, repeated treatment by daily injection (Reneric et al, 2002) or gavage (Kelliher et al, 2003) in rats showed no difference in the behavioral effects with chronic treatment, although this may be a consequence of the doses studied (Detke et al, 1997).…”

Section: Introductionmentioning

confidence: 76%

Behavioral Effects of Chronic Fluoxetine in BALB/cJ Mice Do Not Require Adult Hippocampal Neurogenesis or the Serotonin 1A Receptor

Holick

Lee

Hen

et al. 2007

Neuropsychopharmacol

277

206

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We previously reported that chronic, but not subchronic, treatment with the selective serotonin reuptake inhibitor (SSRI) fluoxetine altered behavior in the forced swimming test (FST) in BALB/cJ mice. We now use this model to investigate mechanisms underlying the delayed onset of the behavioral response to antidepressants, specifically (1) adult hippocampal neurogenesis and (2) expression of the 5-HT1A receptor. Here, we show data validating this model of chronic antidepressant action. We found the FST to be selectively responsive to chronic administration of the SSRI fluoxetine (18 mg/kg/day) and the tricyclic antidepressant desipramine (20 mg/kg/day), but not to the antipsychotic haloperidol (1 mg/kg/day) in BALB/cJ mice. The behavioral effects of fluoxetine emerged by 12 days of treatment, and were affected neither by ablation of progenitor cells of the hippocampus nor by genetic deletion of the 5-HT1A receptor. The effect of fluoxetine in the BALB/cJ mice was also neurogenesis-independent in the novelty-induced hypophagia test. We also found that chronic fluoxetine does not induce an increase in cell proliferation or the number of young neurons as measured by BrdU and doublecortin immunolabeling, respectively, in BALB/cJ mice. These data are in contrast to our previous report using a different strain of mice (129SvEvTac). In conclusion, we find that BALB/cJ mice show a robust response to chronic SSRI treatment in the FST, which is not mediated by an increase in new neurons in the hippocampus, and does not require the 5-HT1A receptor. These findings suggest that SSRIs can produce antidepressant-like effects via distinct mechanisms in different mouse strains.

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Section: Introductionmentioning

confidence: 76%

Behavioral Effects of Chronic Fluoxetine in BALB/cJ Mice Do Not Require Adult Hippocampal Neurogenesis or the Serotonin 1A Receptor

Holick

Lee

Hen

et al. 2007

Neuropsychopharmacol

277

206

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“…However, acute antidepressant-like effects in the forced swim test are likely to reflect the initial events elicited by antidepressants rather than the progressive changes that are likely to accompany chronic antidepressant treatment. Studies comparing the acute and chronic effects of SSRIs in the forced swim test have reported comparable behavioral effects at the two timepoints both in rats (Reneric et al, 2002;Kelliher et al, 2003) and in mice (Conti et al, 2002). In addition, C57BL/6 mice have been shown to be sensitive to chronic treatment with tricyclic antidepressants in the forced swim test, although acute or subchronic timepoints were not evaluated (Alcaro et al, 2002).…”

Section: Discussionmentioning

confidence: 99%

“…Only one report has found antidepressant effects of chronic, but not acute, low dose fluoxetine or desipramine treatment in rats (Detke et al, 1997). Furthermore, the dual 5-HT/NA reuptake inhibitor milnacipran has been shown to increase climbing when given subchronically, and increase both climbing and swimming when given chronically in rats (Reneric et al, 2002). Here, we observed that while subchronic fluoxetine had no effect, chronic treatment with 10 and 18 mg/kg/day fluoxetine increased swimming and reduced immobility in both experiments in BALB/c mice (Figures 1 and 6).…”

Section: Discussionmentioning

confidence: 99%

Effects of Chronic Fluoxetine in Animal Models of Anxiety and Depression

Dulawa

Holick

Gundersen

et al. 2004

Neuropsychopharmacol

610

485

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The onset of the therapeutic response to antidepressant treatment exhibits a characteristic delay. Animal models sensitive to chronic, but not acute, antidepressant treatment are greatly needed for studying antidepressant mechanisms. We initially assessed four inbred mouse strains for their behavioral response to chronic treatment with the selective-serotonin reuptake inhibitor fluoxetine (0, 5, 10 mg/kg/day in drinking water), which is used for the treatment of mood and anxiety disorders. Only the highly anxious BALB/c strain exhibited sensitivity to fluoxetine in the forced swim test. Additionally, fluoxetine reduced locomotion in C57BL/6 and 129SvEv, but not BALB/c and DBA/2, strains. We then evaluated the effects of subchronic (B4 days) and chronic (B24 days) fluoxetine treatment (0, 10, 18, 25 mg/kg/day) on measures of anxiety and depression in BALB/c mice. Anxiety measures were obtained using the open field and noveltyinduced hypophagia tests. Antidepressant effects were evaluated using the forced swim test. We found 18 mg/kg/day of chronic fluoxetine to be active in all three paradigms; subchronic treatment had no effect. Anxiety-related measures were reduced by 18 mg/kg/ day. In the forced swim test, 10 and 18 mg/kg/day increased swimming and reduced immobility. Here we present several novel effects of chronic, but not subchronic, antidepressant treatment.

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“…Swimming sessions were conducted by placing rats in individual Plexiglas cylinders (46 cm tall Â 20 cm in diameter), filled with water (23)(24)(25) C) up to 30 cm from bottom. All swimming sessions were carried out between 12:00 and 18:00 h.…”

Section: Antidepressant Activitymentioning

confidence: 99%

Biological activities of Zn(II)-S-methyl-cysteine complex as antiradical, inhibitor of acid phosphatase enzyme and in vivo antidepressant effects

Escudero¹,

Martini

Jori

et al. 2016

Journal of Enzyme Inhibition and Medicinal Chemistry

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The antidepressant effect of simple Zn(II) salts has been proved in several animal models of depression. In this study, a coordination metal complex of Zn(II) having a sulfur containing ligand is tested as antidepressant for the first time. Forced swimming test method on male Wistar rats shows a decrease in the immobility and an increase in the swimming behavior after treatment with [Zn(S-Met) 2 ] (S-Met¼S-methyl-L-cysteine) being more effective and remarkable than ZnCl 2 . The thiobarbituric acid and the pyranine consumption (hydroxyl and peroxyl radicals, respectively) methods were applied to evaluate the antioxidant activity of S-Met and [Zn(S-Met) 2 ] showing evidence of attenuation of hydroxyl but not peroxyl radicals activities. UVvis studies on the inhibition of acid phosphatase enzyme (AcP) demonstrated that S-methyl-Lcysteine did not produce any effect but, in contrast, [Zn(S-Met) 2 ] complex behaved as a moderate inhibitor. Finally, bioavailability studies were performed by fluorescence spectroscopy denoting the ability of the albumin to transport the complex.

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In the rat forced swimming test, chronic but not subacute administration of dual 5-HT/NA antidepressant treatments may produce greater effects than selective drugs

Cited by 71 publications

References 53 publications

Behavioral Effects of Chronic Fluoxetine in BALB/cJ Mice Do Not Require Adult Hippocampal Neurogenesis or the Serotonin 1A Receptor

Behavioral Effects of Chronic Fluoxetine in BALB/cJ Mice Do Not Require Adult Hippocampal Neurogenesis or the Serotonin 1A Receptor

Effects of Chronic Fluoxetine in Animal Models of Anxiety and Depression

Biological activities of Zn(II)-S-methyl-cysteine complex as antiradical, inhibitor of acid phosphatase enzyme and in vivo antidepressant effects

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