SONU20176289, a compound combining partial dopamine D2 receptor agonism with specific serotonin reuptake inhibitor activity, affects neuroplasticity in an animal model for depression

Michael‐Titus, Adina T.; Albert, M.; Michael, Gregory J.; Michaelis, Thomas; Watanabe, Takashi; Frahm, Jens; Pudovkina, Olga L.; Hart, Marieke G. C. van der; Hesselink, Mayke B.; Fuchs, Eberhard; Czéh, Boldizsár

doi:10.1016/j.ejphar.2008.09.006

Cited by 15 publications

(10 citation statements)

References 64 publications

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“…For example, it has been suggested that the serotoninergic pathway is involved in the affective state of sheep (Doyle et al 2011). MRI techniques could be used to investigate the impact of various neurobiological factors on emotional state, as shown in pharmacological models of depression (Michael-Titus et al 2008). More interestingly, we propose the use of large animal models to study the long-term effects of strong acute emotion in prenatal or perinatal life on brain development and behaviour.…”

Section: Emotional Reactionmentioning

confidence: 99%

MRI Techniques and New Animal Models for Imaging the Brain

Chaillou¹,

Tillet²,

Andersson³

2012

When Things Go Wrong - Diseases and Disorders of the Human Brain

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Section: Emotional Reactionmentioning

confidence: 99%

MRI Techniques and New Animal Models for Imaging the Brain

Chaillou¹,

Tillet²,

Andersson³

2012

When Things Go Wrong - Diseases and Disorders of the Human Brain

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“…Early life stress may underlie the reduced hippocampal volumes observed in some patients with MDD (see Frodl and O'Keane, in press for review). Efficacious antidepressant treatments function in part, by normalizing disturbed neuroplasticity (Michael-Titus et al, 2008) and facilitating axonal and dendritic sprouting (Vaidya et al, 1999) — processes that can help restore synaptic connections within the neuropil. Although the role of hippocampal neurogenesis in the development and persistence of depression is not completely understood, its requirement for antidepressant efficacy is well accepted (Lewitus et al, 2009; Santarelli et al, 2003; Malberg et al, 2000).…”

Section: Introductionmentioning

confidence: 99%

Adipocytokine signaling is altered in flinders sensitive line rats, and adiponectin correlates in humans with some symptoms of depression

Wilhelm¹,

Choi²,

Huckans³

et al. 2013

Pharmacology Biochemistry and Behavior

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Major depression is a complex multi-factorial disorder with a lifetime diagnosis of nearly 1 out of 6. We used the Flinders Sensitive Line (FSL) of rats, a model of depression, and the parent Sprague–Dawley (SD) rats to identify genes, gene ontology categories and pathways associated with depression. Depression-like behavior was verified in the FSL line by forced swim testing, with FSL animals exhibiting greater immobility compared to SD rats. RNA samples from the hippocampus were isolated from a group of experimentally naïve FSL and SD rats for microarray analysis. Microarray analysis yielded a total of 361 genes that were differentially regulated between FSL and SD rats, with catechol-O-methyltransferase (COMT) being the most up-regulated. The genes that were differentially regulated between FSL and SD rats were subjected to bioinformatic analysis using the Database for Annotation, Visualization and Integrated Discovery (DAVID), which yielded several gene ontology categories that were overrepresented. Subsequent pathway analysis indicated dysregulation of the adipocytokine signaling pathway. To test the translational impact of this pathway, metabolic factors and psychiatric symptoms were evaluated in a sample of human research participants. Results from our human subjects indicated that anxiety and a subset of depressive symptoms were correlated with adiponectin levels (but not leptin levels). Our results and those of others suggest that disruption of the adipocytokine signaling pathway may be a critical component of the depressive-like behaviors observed in the FSL rats and may also be an important indicator of depressive and anxiety symptoms in humans.

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“…Drugs prescribed to treat depression, such as paroxetine, fluoxetine, and imipramine, alter brain- and mitochondrial-type creatine kinases in the prefrontal cortex, hippocampus, and striatum (Agostinho et al, 2009; Assis et al, 2009; Santos et al, 2009), areas of the brain known to be involved with depression (Drevets et al, 2008; Maletic et al, 2007). Additionally, antidepressant drugs increase creatine and phosphocreatine concentrations in the prefrontal cortex and hippocampus in animal models of depression (Kim et al, 2010; Czéh et al, 2001; Michael-Titus et al, 2008). It is hypothesized that increased phosphocreatine stores and creatine kinase activity attenuate metabolic impairments associated with depression by increasing the rate of ATP replenishment and accordingly improving neuronal integrity or function (Agostinho et al, 2009; Kim et al, 2010; Santos et al, 2009).…”

Section: Introductionmentioning

confidence: 99%

Sex-specific antidepressant effects of dietary creatine with and without sub-acute fluoxetine in rats

Allen

D’Anci

Kanarek

et al. 2012

Pharmacology Biochemistry and Behavior

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The potential role of metabolic impairments in the pathophysiology of depression is motivating researchers to evaluate the treatment efficacy of creatine, a naturally occurring energetic and neuroprotective compound found in brain and muscle tissues. Growing evidence is demonstrating the benefit of oral creatine supplements for reducing depressive symptoms in humans and animals. A novel question is whether dietary creatine, when combined with antidepressant drug therapy, would be more effective than either compound alone. To answer this question, four studies were conducted to investigate the behavioral effects of combined creatine and low-dose fluoxetine treatment using the forced swim test in male and female rats. Sprague-Dawley rats were fed powdered rodent chow supplemented with 0%, 2% or 4% w/w creatine monohydrate for 5 weeks. Rats were injected with fluoxetine (5.0 or 10.0 mg/kg) or saline according to a sub-acute dosing schedule. Female rats maintained on a 4% creatine diet displayed antidepressant-like effects compared to non-supplemented females prior to fluoxetine treatment. In contrast, creatine did not alter behavior reliably in males. Following drug treatment and a second forced swim trial, the antidepressant-like profile of creatine remained significant only in females co-administered 5.0 mg/kg fluoxetine. Moreover, in females only, supplementation with 4% creatine produced a more robust antidepressant-like behavioral profile compared to either dose of fluoxetine alone. Estrous cycle data indicated that ovarian hormones influenced the antidepressant-like effects of creatine. Addressing the issue of sex differences in response to treatment may affect our understanding of creatine, its relationship with depressive behavior, and may lead to sex-specific therapeutic strategies.

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SONU20176289, a compound combining partial dopamine D2 receptor agonism with specific serotonin reuptake inhibitor activity, affects neuroplasticity in an animal model for depression

Cited by 15 publications

References 64 publications

MRI Techniques and New Animal Models for Imaging the Brain

MRI Techniques and New Animal Models for Imaging the Brain

Adipocytokine signaling is altered in flinders sensitive line rats, and adiponectin correlates in humans with some symptoms of depression

Sex-specific antidepressant effects of dietary creatine with and without sub-acute fluoxetine in rats

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