Recent advances in animal models of chronic antidepressant effects: The novelty-induced hypophagia test

Dulawa, Stephanie C.; Hen, René

doi:10.1016/j.neubiorev.2005.03.017

Cited by 376 publications

(318 citation statements)

References 112 publications

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“…3A,B). As anxiolytic drugs are well-documented to increase noveltysuppressed consummatory behaviour (Loiseau et al, 2003;Dulawa and Hen, 2005) and the anxiolytic effects of dimebon were observed in two classical tests for anxiety-like behaviour and open field tests (Bachurin and Grigoriev, 2009), our findings might be considered to be an indication of the anti-anxiety properties of dimebon. In the latter study, bolus intraperitoneal administration of dimebon at a dose of 2 mg/kg, 40 min prior to testing was found to induce an anxiolytic effect in a rat Vogel conflict model, dark/light box paradigm, and an open field test, that was similar to the effects of diazepam applied at the same dose.…”

Section: Discussionsupporting

confidence: 62%

“…Starting from day 4, trial 2 and until the end of the training period, the duration of drinking did not differ between groups (p N 0.05, Mann-Whitney U test). Thus, in a novel environment, which is well documented to induce anxiety and suppress consummatory behaviour (Loiseau et al, 2003;Dulawa and Hen, 2005), mice repeatedly treated with dimebon showed elevated water intake. The latter finding suggested that drug administration might induce an anxiolytic-like effect and/or change the physiological need for water.…”

Section: Repeated Dimebon Administration Enhances Learning In the Y-mazementioning

confidence: 99%

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Dimebon enhances hippocampus-dependent learning in both appetitive and inhibitory memory tasks in mice

Vignisse

Steinbusch

Bolkunov

et al. 2011

Progress in Neuro-Psychopharmacology and Biological Psychiatry

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a b s t r a c t a r t i c l e i n f oPre-clinical and clinical studies on dimebon (dimebolin or latrepirdine) have demonstrated its use as a cognitive enhancer. Here, we show that dimebon administered to 3-month-old C57BL6N mice 15 min prior to training in both appetitive and inhibitory learning tasks via repeated (0.1 mg/kg) and acute (0.5 mg/kg) i.p. injections, respectively, increases memory scores. Acute treatment with dimebon was found to enhance inhibitory learning, as also shown in the step-down avoidance paradigm in 7-month-old mice. Bolus administration of dimebon did not affect the animals' locomotion, exploration or anxiety-like behaviour, with the exception of exploratory behaviour in older mice in the novel cage test. In a model of appetitive learning, a spatial version of the Y-maze, dimebon increased the rate of correct choices and decreased the latency of accessing a water reward after water deprivation, and increased the duration of drinking behaviour during training/testing procedures. Repeated treatment with dimebon did not alter the behaviours in other tests or water consumption. Acute treatment of water-deprived and non-water-deprived mice with dimebon also did not affect their water intake. Our data suggest that dimebon enhances hippocampus-dependent learning in both appetitive and inhibitory tasks in mice.

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Section: Discussionsupporting

confidence: 62%

Section: Repeated Dimebon Administration Enhances Learning In the Y-mazementioning

confidence: 99%

Dimebon enhances hippocampus-dependent learning in both appetitive and inhibitory memory tasks in mice

Vignisse

Steinbusch

Bolkunov

et al. 2011

Progress in Neuro-Psychopharmacology and Biological Psychiatry

View full text Add to dashboard Cite

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“…76 While it is a valid point that the forced swim test, used in a majority of such studies, suffers considerable limitations in terms of construct and face validity, the authors fail to mention these limitations when the same paradigm has been cited in support of their neurotrophic hypothesis. 30,76 Studies utilizing alternative assays, such as novelty-induced hypophagia and chronic social defeat, 18,77 will be important in determining the strength of this argument. Furthermore, while a loss of BDNF may not generate spontaneous depressive traits, it may represent a predisposing factor, and a manipulation such as chronic stress is necessary for its manifestation and subsequent detection.…”

Section: Can Genetically Altered Mice Help?mentioning

confidence: 99%

Is it time to reassess the BDNF hypothesis of depression?

2007

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The brain-derived neurotrophic factor (BDNF) hypothesis of depression postulates that a loss of BDNF is directly involved in the pathophysiology of depression, and that its restoration may underlie the therapeutic efficacy of antidepressant treatment. While this theory has received considerable experimental support, an increasing number of studies have generated evidence which is not only inconsistent, but also directly contradicts the hypothesis. This article provides a critical review of the clinical and preclinical studies which have been responsible for this controversy, outlining pharmacological, behavioural and genetic evidence which demonstrates the contrasting role of BDNF in regulating mood and antidepressant effects throughout the brain. I will also review key studies, both human and animal, which have investigated the association of a BDNF single-nucleotide polymorphism (Val66Met) with depression pathogenesis, and detail the number of inconsistencies which also afflict this novel area of BDNF research. The article will conclude by discussing why now is a critical time to reassess the original BDNF hypothesis of depression, and look towards the formation of new models that can provide a more valid account of the complex relationships between growth factors, mood disorders and their treatment.

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“…Thus, for the functional validation of some transcripts identified as possible drug targets, further studies will be necessary to assess the effect of transcriptional regulation in one or more rodent models of depression. [38][39][40][41][42][43] Another apparent limitation is that transcriptional profiles for the different treatments were compared only at the time points corresponding to clinical efficacy, which differed for each treatment being 2 days for ECT, 1 day for SD and 14 days for FLX. Thus, a comparative analysis of transcriptional changes induced at the same time points for all treatments is missing.…”

Section: Number Of Transcripts Affected By Single and Multiple Treatmmentioning

confidence: 99%

Region-specific transcriptional changes following the three antidepressant treatments electro convulsive therapy, sleep deprivation and fluoxetine

et al. 2006

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The significant proportion of depressed patients that are resistant to monoaminergic drug therapy and the slow onset of therapeutic effects of the selective serotonin reuptake inhibitors (SSRIs)/serotonin/noradrenaline reuptake inhibitors (SNRIs) are two major reasons for the sustained search for new antidepressants. In an attempt to identify common underlying mechanisms for fast-and slow-acting antidepressant modalities, we have examined the transcriptional changes in seven different brain regions of the rat brain induced by three clinically effective antidepressant treatments: electro convulsive therapy (ECT), sleep deprivation (SD), and fluoxetine (FLX), the most commonly used slow-onset antidepressant. Each of these antidepressant treatments was applied with the same regimen known to have clinical efficacy: 2 days of ECT (four sessions per day), 24 h of SD, and 14 days of daily treatment of FLX, respectively. Transcriptional changes were evaluated on RNA extracted from seven different brain regions using the Affymetrix rat genome microarray 230 2.0. The gene chip data were validated using in situ hybridization or autoradiography for selected genes. The major findings of the study are:1. The transcriptional changes induced by SD, ECT and SSRI display a regionally specific distribution distinct to each treatment. 2. The fast-onset, short-lived antidepressant treatments ECT and SD evoked transcriptional changes primarily in the catecholaminergic system, whereas the slow-onset antidepressant FLX treatment evoked transcriptional changes in the serotonergic system. 3. ECT and SD affect in a similar manner the same brain regions, primarily the locus coeruleus, whereas the effects of FLX were primarily in the dorsal raphe and hypothalamus, suggesting that both different regions and pathways account for fast onset but short lasting effects as compared to slow-onset but long-lasting effects. However, the similarity between effects of ECT and SD is somewhat confounded by the fact that the two treatments appear to regulate a number of transcripts in an opposite manner. 4. Multiple transcripts (e.g. brain-derived neurotrophic factor (BDNF), serum/glucocorticoidregulated kinase (Sgk1)), whose level was reported to be affected by antidepressants or behavioral manipulations, were also found to be regulated by the treatments used in the present study. Several novel findings of transcriptional regulation upon one, two or all three treatments were made, for the latter we highlight homer, erg2, HSP27, the proto oncogene ret, sulfotransferase family 1A (Sult1a1), glycerol 3-phosphate dehydrogenase (GPD3), the orphan receptor G protein-coupled receptor 88 (GPR88) and a large number of expressed sequence tags (ESTs). 5. Transcripts encoding proteins involved in synaptic plasticity in the hippocampus were strongly affected by ECT and SD, but not by FLX.The novel transcripts, concomitantly regulated by several antidepressant treatments, may represent novel targets for fast onset, long-duration antidepressants.

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Recent advances in animal models of chronic antidepressant effects: The novelty-induced hypophagia test

Cited by 376 publications

References 112 publications

Dimebon enhances hippocampus-dependent learning in both appetitive and inhibitory memory tasks in mice

Dimebon enhances hippocampus-dependent learning in both appetitive and inhibitory memory tasks in mice

Is it time to reassess the BDNF hypothesis of depression?

Region-specific transcriptional changes following the three antidepressant treatments electro convulsive therapy, sleep deprivation and fluoxetine

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