Immunohistochemical study of the serotonergic neuronal system in an animal model of the mood disorder

Iritani, Shuji; Tohgi, Mizuho; Arai, Tetsuaki; Ikeda, Kenji

doi:10.1016/j.expneurol.2006.03.013

Cited by 20 publications

(10 citation statements)

References 31 publications

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“…Reserpine can induce depression-like behaviors in animals by depletion of catecholamine and blocking reuptake. This animal model has been used for investigating the underlying mechanism of depression [26, 27]. …”

Section: Introductionmentioning

confidence: 99%

Subchronic Arsenic Exposure Induces Anxiety-Like Behaviors in Normal Mice and Enhances Depression-Like Behaviors in the Chemically Induced Mouse Model of Depression

Chang

Guo

Tsai

et al. 2015

BioMed Research International

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Accumulating evidence implicates that subchronic arsenic exposure causes cerebral neurodegeneration leading to behavioral disturbances relevant to psychiatric disorders. However, there is still little information regarding the influence of subchronic exposure to arsenic-contaminated drinking water on mood disorders and its underlying mechanisms in the cerebral prefrontal cortex. The aim of this study is to assess the effects of subchronic arsenic exposure (10 mg/LAs2O3 in drinking water) on the anxiety- and depression-like behaviors in normal mice and in the chemically induced mouse model of depression by reserpine pretreatment. Our findings demonstrated that 4 weeks of arsenic exposure enhance anxiety-like behaviors on elevated plus maze (EPM) and open field test (OFT) in normal mice, and 8 weeks of arsenic exposure augment depression-like behaviors on tail suspension test (TST) and forced swimming test (FST) in the reserpine pretreated mice. In summary, in this present study, we demonstrated that subchronic arsenic exposure induces only the anxiety-like behaviors in normal mice and enhances the depression-like behaviors in the reserpine induced mouse model of depression, in which the cerebral prefrontal cortex BDNF-TrkB signaling pathway is involved. We also found that eight weeks of subchronic arsenic exposure are needed to enhance the depression-like behaviors in the mouse model of depression. These findings imply that arsenic could be an enhancer of depressive symptoms for those patients who already had the attribute of depression.

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Section: Introductionmentioning

confidence: 99%

Subchronic Arsenic Exposure Induces Anxiety-Like Behaviors in Normal Mice and Enhances Depression-Like Behaviors in the Chemically Induced Mouse Model of Depression

Chang

Guo

Tsai

et al. 2015

BioMed Research International

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“…Importantly, like others (24) we did not detect differences in the distribution of OCT3 immunostaining in the hippocampus among 5-HTT genotypes, indicating that the cellular distribution of OCT3 does not change as a function of 5-HTT genotype. In WT and 5-HTT ϩ/Ϫ mice, 5-HTTs are also expressed in these hippocampal layers (15,30,31). Thus, OCT3 is also positioned in the proximity of 5-HT terminals and therefore OCT3 could increase its contribution to 5-HT clearance when 5-HTT expression and/or function are compromised.…”

mentioning

confidence: 99%

Organic cation transporter 3: Keeping the brake on extracellular serotonin in serotonin-transporter-deficient mice

Baganz

Horton

Calderon

et al. 2008

Proc. Natl. Acad. Sci. U.S.A.

155

173

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Mood disorders cause much suffering and are the single greatest cause of lost productivity worldwide. Although multiple medications, along with behavioral therapies, have proven effective for some individuals, millions of people lack an effective therapeutic option. A common serotonin (5-HT) transporter (5-HTT/SERT, SLC6A4) polymorphism is believed to confer lower 5-HTT expression in vivo and elevates risk for multiple mood disorders including anxiety, alcoholism, and major depression. Importantly, this variant is also associated with reduced responsiveness to selective 5-HT reuptake inhibitor antidepressants. We hypothesized that a reduced antidepressant response in individuals with a constitutive reduction in 5-HTT expression could arise because of the compensatory expression of other genes that inactivate 5-HT in the brain. A functionally upregulated alternate transporter for 5-HT may prevent extracellular 5-HT from rising to levels sufficiently high enough to trigger the adaptive neurochemical events necessary for therapeutic benefit. Here we demonstrate that expression of the organic cation transporter type 3 (OCT3, SLC22A3), which also transports 5-HT, is upregulated in the brains of mice with constitutively reduced 5-HTT expression. Moreover, the OCT blocker decynium-22 diminishes 5-HT clearance and exerts antidepressantlike effects in these mice but not in WT animals. OCT3 may be an important transporter mediating serotonergic signaling when 5-HTT expression or function is compromised.5HTTLPR ͉ antidepressant ͉ polymorphism ͉ hippocampus ͉ chronamperometry

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“…Joh et al reported that the effects of reserpine on the adrenal glands resemble that of psychological stress 2 . This animal model has been used for investigating the underlying mechanism of psychological stress/depression 10 , 11 , 12 …”

Section: Introductionmentioning

confidence: 66%

Reserpine‐induced model of stress suppresses mucosal immunity

et al. 2006

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Summary Stress contributes significantly to the development of many diseases. In clinical studies, a strong correlation between depression and immune dysfunction has been shown. Our previous studies indicated that sympathetic innervation can regulate intestinal mucosal immunity through sympathetic synapses, but the mechanism in stress/ depression-induced intestinal immune deficiency was unclear. Using a mouse model in which behavioural stress/ depression is chemically induced by reserpine, it is found that there is a substantial deficiency of intestinal local humoral and particularly specific antibody response to the antigen stimulation in reserpine-treated group. No significant difference of CD4 1 , CD8 1 or Mac1 1 cells between reserpine-treated and control groups was detected in the intestine. This deficiency is closely correlated with stress/depression. A possible correlation between stress, cytokine secretion and humoral immunity in vivo is postulated.

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Immunohistochemical study of the serotonergic neuronal system in an animal model of the mood disorder

Cited by 20 publications

References 31 publications

Subchronic Arsenic Exposure Induces Anxiety-Like Behaviors in Normal Mice and Enhances Depression-Like Behaviors in the Chemically Induced Mouse Model of Depression

Subchronic Arsenic Exposure Induces Anxiety-Like Behaviors in Normal Mice and Enhances Depression-Like Behaviors in the Chemically Induced Mouse Model of Depression

Organic cation transporter 3: Keeping the brake on extracellular serotonin in serotonin-transporter-deficient mice

Reserpine‐induced model of stress suppresses mucosal immunity

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