Modulation of the suppressive effect of corticosterone on adult rat hippocampal cell proliferation by paroxetine

Qiu, Guang; Helmeste, Daiga M.; Samaranayake, Asanka N.; Lau, Benson Wui-Man; Lee, Tatia M.C.; Tang, Siu Wa; So, Kwok-Fai

doi:10.1007/s12264-007-0019-9

Cited by 38 publications

(34 citation statements)

References 22 publications

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“…In agreement with previous findings (David et al 2009 ;Murray et al 2008 ;Qiu et al 2007), we found a reduction in the proliferation of progenitor cells after chronic corticosterone treatment was observed (Fig. 5), emphasizing a role for glucocorticoids in the regulation of the proliferation stage of the neurogenic process.…”

Section: Discussionsupporting

confidence: 93%

Beneficial behavioural and neurogenic effects of agomelatine in a model of depression/anxiety

Rainer

Xia

Guilloux

et al. 2011

Int. J. Neuropsychopharm.

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Agomelatine (S20098) is a novel antidepressant drug with melatonergic agonist and 5-HT2C receptor antagonist properties, displaying antidepressant/anxiolytic-like properties in animal models and in humans. In a depression/anxiety-like mouse model in which the response of the HPA axis is blunted, we investigated whether agomelatine could reverse behavioural deficits related to depression/anxiety compared to the classical selective serotonin reuptake inhibitor, fluoxetine. Adult mice were treated for 8 wk with either vehicle or corticosterone (35 μg/ml.d) via drinking water. During the final 4 wk, animals were treated with vehicle, agomelatine (10 or 40 mg/kg i.p.) or fluoxetine (18 mg/kg i.p.) and tested in several behavioural paradigms and also evaluated for home-cage activity. Our results showed that the depressive/anxiety-like phenotype induced by corticosterone treatment is reversed by either chronic agomelatine or fluoxetine treatment. Moreover, agomelatine increased the dark/light ratio of home-cage activity in vehicle-treated mice and reversed the alterations in this ratio induced by chronic corticosterone, suggesting a normalization of disturbed circadian rhythms. Finally, we investigated the effects of this new antidepressant on neurogenesis. Agomelatine reversed the decreased cell proliferation in the whole hippocampus in corticosterone-treated mice and increased maturation of newborn neurons in both vehicle- and corticosterone-treated mice. Overall, the present study suggests that agomelatine, with its distinct mechanism of action based on the synergy between the melatonergic agonist and 5-HT2C antagonist properties, provides a distinct antidepressant/anxiolytic spectrum including circadian rhythm normalization.

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Section: Discussionsupporting

confidence: 93%

Beneficial behavioural and neurogenic effects of agomelatine in a model of depression/anxiety

Rainer

Xia

Guilloux

et al. 2011

Int. J. Neuropsychopharm.

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“…The neurogenesis hypothesis of depression has been supported by studies showing that while stress inhibits neurogenesis (Alonso et al 2004;Mineur et al 2007), many classes of antidepressants enhance it in the SGZ of the hippocampus (Malberg et al 2000;Santarelli et al 2003;Warner-Schmidt and Duman 2006;Qiu et al 2007). In addition, with a few recent exceptions (David et al 2009;Bessa et al 2009), reversal of depressive-like behaviours by antidepressants has been associated with hippocampal neurogenesis (Santarelli et al 2003;Jayatissa et al 2006;Czeh and Lucassen 2007;Kong et al 2009).…”

Section: Short-versus Long-term Cell Proliferation and Neurogenesismentioning

confidence: 99%

Sustained stress-induced changes in mice as a model for chronic depression

et al. 2010

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“…The dosage of drugs was shown to be effective in suppressing/ increasing neurogenesis [9,10]. Twenty-four hours after the last dose of drug delivery, the animals were subjected to PPI test.…”

Section: Drug Treatments and Exercise Trainingmentioning

confidence: 99%

Intracerebroventricular infusion of cytosine-arabinoside causes prepulse inhibition disruption

et al. 2009

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Adult neurogenesis in hippocampus is associated with behaviors such as learning. Hippocampus is involved in the regulation of prepulse inhibition (PPI), but the relationship between neurogenesis and PPI is unexplored. We conducted four experiments to determine the role of neural progenitor cell proliferation in PPI. Intracerebroventricular infusion of cytostatic cytosine arabinoside caused PPI disruption but repeated exposure to PPI sessions prevented the PPI disruption. Corticosterone treatment, which decreases hippocampal cell proliferation, caused PPI disruption, whereas antidepressant and exercise, which increased cell proliferation, did not affect PPI. These results suggest that cell proliferation is involved in the first encounter with PPI test while its importance may decrease upon repeated exposures to the tests.

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Modulation of the suppressive effect of corticosterone on adult rat hippocampal cell proliferation by paroxetine

Abstract: This may have clinic application in preventing hippocampal damage after glucocorticoid treatment.

Cited by 38 publications

References 22 publications

Beneficial behavioural and neurogenic effects of agomelatine in a model of depression/anxiety

Beneficial behavioural and neurogenic effects of agomelatine in a model of depression/anxiety

Sustained stress-induced changes in mice as a model for chronic depression

Intracerebroventricular infusion of cytosine-arabinoside causes prepulse inhibition disruption

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