Repeated clomipramine treatment reversed the inhibition of cell proliferation in adult hippocampus induced by chronic unpredictable stress

Liu, Qiong; Yu, Jin; Mao-Ying, Qi-Liang; Mi, Wen-Li; Li, Bo; Wang, Yan-Qing; Wang, Ji‐Jiang; Wu, Gen-Cheng

doi:10.1038/sj.tpj.6500485

Cited by 32 publications

(32 citation statements)

References 46 publications

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“…Although the relationship between stressors such as IM and NC remains controversial, the "antistress" effects of NC have been reported against the IM-enhanced activity of the sympathetic nervous system (Yoshida et al, 1994;Serova et al, 1999), and this may be correlated with the attenuated anhedonia in of NC against the IM-induced depression-like behavioral alterations in the other two tests may be due to the differences in the mechanisms underlying anhedonia and other depression-related symptoms, as previously suggested (Liu et al, 2008;Jayatissa et al, 2010). Furthermore, the absence of stress-NC interactions has also been reported for alterations in locomotor activity and corticosterone release in a rat experimental model (Cruz et al, 2008), -cations against some of the behavioral effects of IM.…”

Section: Im-and/or Nc-induced Depression-like Behavioral Alterationsmentioning

confidence: 61%

“…4 days) did not cause any anhedonic behavioral alterations, presumably due to the absence of withdrawal-like impairments in dopamine reuptake (Paterson et al, 2007). Previous studies have suggested that there are differences in the mechanisms responsible for anhedonia and other depression-related symptoms, based on differences such as differential cell proliferation in the hippocampus (Liu et al, 2008;Jayatissa et al, 2010). Therefore, it is possible that NC, unlike IM, could modify the mechanisms of each component of the depression-related behavioral alterations differently.…”

Section: Im-and/or Nc-induced Depression-like Behavioral Alterationsmentioning

confidence: 91%

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Depression-related anhedonic behaviors caused by immobilization stress: a comparison with nicotine-induced depression-like behavioral alterations and effects of nicotine and/or "antidepressant" drugs

Hayase

2011

J. Toxicol. Sci.

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-Anhedonia, an affective symptom related to the inability to experience pleasure, is one of the representative symptoms observed in depression. In the present study, considering that repeated nicotine (NC) also causes "depressive" symptoms, the depression-related anhedonic behavioral alterations caused by a typical depression-inducing stressor, immobilization stress (IM), combined with or without NC administration, were examined in mice and compared with the depression-like behavioral alterations caused by NC. In the repeated IM (10 min, 4 days) group, as well as the repeated NC (0.3 mg/kg, s.c., 4 days) group, depression-related behavioral despair was observed in both forced swimming and tail suspension tests. Depression-related anhedonic behavioral alterations, as judged in the sucrose test, were observed only in the IM group. In the group treated with IM plus NC (IM-NC group), NC antagonized the IM-induced anhedonic attenuation of sucrose consumption in the sucrose test. Furthermore, in the IM-NC group, NC attenuated the effects of antidepressants which inhibit the reuptake of monoamines in the forced swimming test. Against the IM-induced anhedonia in the sucrose test, the cannabinoid agonists anandamide and CP 55940, in addition to the antidepressants previously reported, restored the preference for sucrose to control levels, with or without NC co-treatment. The absence of anhedonic behavioral alterations, the antidepressant-like anti-anhedonic effects against IM, and the effects against some antidepressant drugs all seemed to be characteristic of the effects of NC. Neural mechanisms other than those involved in the depression-like effects of NC seemed to contribute to the IM-induced anhedonic component of depression.

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Section: Im-and/or Nc-induced Depression-like Behavioral Alterationsmentioning

confidence: 61%

Section: Im-and/or Nc-induced Depression-like Behavioral Alterationsmentioning

confidence: 91%

Depression-related anhedonic behaviors caused by immobilization stress: a comparison with nicotine-induced depression-like behavioral alterations and effects of nicotine and/or "antidepressant" drugs

Hayase

2011

J. Toxicol. Sci.

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“…Finally, the prevailing perception in the literature, suggests FST to be a proper test to show neurogenesis-dependence of antidepressant efficacy. Several groups described X-irradiation to block antidepressant effects using FST (e.g., Zhu et al, 2010;Garza et al, 2012) while correlative observations linking antidepressant treatment effects in FST and adult hippocampal neurogenesis have been reported numerous times (Liu et al, 2008;Silva et al, 2008;Schmidt and Duman, 2010;Wainwright et al, 2011;Wang et al, 2011;Jiang et al, 2012;Lin and Wang, 2014;Lu et al, 2014).…”

Section: Discussionmentioning

confidence: 99%

Mice with ablated adult brain neurogenesis are not impaired in antidepressant response to chronic fluoxetine

Jedynak

Kos

Sandi

et al. 2014

Journal of Psychiatric Research

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a b s t r a c tThe neurogenesis hypothesis of major depression has two main facets. One states that the illness results from decreased neurogenesis while the other claims that the very functioning of antidepressants depends on increased neurogenesis. In order to verify the latter, we have used cyclin D2 knockout mice (cD2 KO mice), known to have virtually no adult brain neurogenesis, and we demonstrate that these mice successfully respond to chronic fluoxetine. After unpredictable chronic mild stress, mutant mice showed depression-like behavior in forced swim test, which was eliminated with chronic fluoxetine treatment, despite its lack of impact on adult hippocampal neurogenesis in cD2 KO mice. Our results suggest that new neurons are not indispensable for the action of antidepressants such as fluoxetine. Using forced swim test and tail suspension test, we also did not observe depression-like behavior in control cD2 KO mice, which argues against the link between decreased adult brain neurogenesis and major depression.

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“…In rodents repeatedly exposed to social defeat, there is a decrease in volume and cell proliferation in the hippocampus that can be reversed by chronic antidepressant treatment (Czéh et al 2007, Becker et al 2008, Van Bokhoven et al 2011). Clomipramine, a tricyclic antidepressant widely used to treat depression and obsessive compulsive disorder, has been shown to reverse the behavioral deficits and inhibition of cell proliferation in the adult hippocampus induced by chronic unpredictable stress (Liu et al 2008(Liu et al , 2012.…”

Section: Introductionmentioning

confidence: 99%

Effects of social stress and clomipramine on emotional memory in mice

Duque¹,

Vinader‐Caerols²,

Monleón³

2016

Acta Neurobiologiae Experimentalis

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We have previously observed impairing effects of social defeat stress (CSDS) on inhibitory avoidance (IA) in mice. Given the similarity between changes produced by social stress in animals and symptoms of certain human psychopathologies such as depression and anxiety, the effects of the antidepressant clomipramine on IA impairment produced by CSDS were evaluated in the present study.Male CD1 mice were randomly assigned to the groups: non-stressed+saline, non-stressed+clomipramine, stressed+saline and stressed+clomipramine. Stressed animals were subjected to daily agonistic encounters (10 min) in the home cage of the aggressor over a 20-day period. Just before each encounter, non-stressed and stressed mice were injected i.p. with saline or clomipramine (10 mg/kg) according to their experimental condition. 24 hours after the last CSDS session, all the mice were tested in a step-through IA task. In the IA training phase, animals were punished by a shock to the paw when they entered the dark compartment of the apparatus. In the IA test phase (one week later) the same procedure took place, but without shock. Complementary measures were obtained by evaluating all the animals in an elevated plus maze (locomotor activity and emotionality) and on a hot plate (analgesia). IA learning was confirmed in all groups except the stressed+saline group, which was the only one that exhibited higher anxiety levels. No variations were observed in either locomotor activity or analgesia. In conclusion, CSDS induces anxiety and impairs emotional memory in mice; the negative effects of CSDS on memory appear to be attenuated by clomipramine, and these detrimental effects do not seem to be secondary to the effects of CSDS on locomotor activity, emotionality or pain sensitivity.

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Repeated clomipramine treatment reversed the inhibition of cell proliferation in adult hippocampus induced by chronic unpredictable stress

Cited by 32 publications

References 46 publications

Depression-related anhedonic behaviors caused by immobilization stress: a comparison with nicotine-induced depression-like behavioral alterations and effects of nicotine and/or "antidepressant" drugs

Depression-related anhedonic behaviors caused by immobilization stress: a comparison with nicotine-induced depression-like behavioral alterations and effects of nicotine and/or "antidepressant" drugs

Mice with ablated adult brain neurogenesis are not impaired in antidepressant response to chronic fluoxetine

Effects of social stress and clomipramine on emotional memory in mice

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