Hippocampal synapsin I, growth-associated protein-43, and microtubule-associated protein-2 immunoreactivity in learned helplessness rats and antidepressant-treated rats

Iwata, Masaaki; Shirayama, Yukihiko; Ishida, Hisahito; Kawahara, Ryuzo

doi:10.1016/j.neuroscience.2006.04.060

Cited by 50 publications

(32 citation statements)

References 70 publications

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“…Similar increase of GAP-43 mRNA expression in CA1, CA3 and GCL of the hippocampus was observed following learned helplessness paradigm (Iwata et al, 2006). Learned helplessness paradigm is one of animal models of depression.…”

Section: Discussionsupporting

confidence: 62%

“…Therefore, chronic stress seems to decrease GAP-43 mRNA expression in the hippocampus (Kuroda & McEwen, 1998), however, with some inconsistency (Rosenbrock et al, 2005). Moreover, chronic imipramine and desipramine treatment increase GAP-43 mRNA expression in the hippocampus (Chen et al, 2003;Sairanen et al, 2007), whereas chronic fluoxetine or fluvoxamine treatment tend to decrease GAP-43 mRNA expression (Iwata et al, 2006;Larsen et al, 2008). However, the changes of GAP-43 in the hippocampus by chronic antidepressant treatment in normal laboratory animals may not necessarily reflect the mechanism of antidepressant effect in the depressed animals, since antidepressant treatment in human without depression induces typical side effects rather than antidepressant effect (Nestler et al, 2002).…”

Section: Introductionmentioning

confidence: 97%

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Effects of Repeated Citalopram Treatments on Chronic Mild Stress-Induced Growth Associated Protein-43 mRNA Expression in Rat Hippocampus

Park

Choi

Lee

et al. 2008

Korean J Physiol Pharmacol

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Section: Discussionsupporting

confidence: 62%

Section: Introductionmentioning

confidence: 97%

Effects of Repeated Citalopram Treatments on Chronic Mild Stress-Induced Growth Associated Protein-43 mRNA Expression in Rat Hippocampus

Park

Choi

Lee

et al. 2008

Korean J Physiol Pharmacol

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“…There are a few reports about the effects of antidepressants on synapsin I in rat hippocampus. Chronic treatment with tranylcypromine, but not desipramine or fluoxetine, decreases synapsin I mRNA expression in rat hippocampal DG, CA3, and CA1 (Rapp et al, 2004), and imipramine or fluvoxamine decreases synapsin I immunoreactivity in rat hippocampus (Iwata et al, 2006). Another study showed that injecting rats with lithium for 30 days produces no changes in total synapsin in the hippocampus (Vawter et al, 2002).…”

Section: Discussionmentioning

confidence: 99%

Mifepristone Repairs Region-Dependent Alteration of Synapsin I in Hippocampus in Rat Model of Depression

Han

Wang

et al. 2007

Neuropsychopharmacol

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Clinical investigations present much evidence that the glucocorticoid receptor (GR) antagonist mifepristone leads to a rapid amelioration of depression. The molecular mechanisms of mifepristone involved in the treatment of depression are not fully understood. Depression is associated with hippocampal plasticity, for which increased excitatory amino acid (EAA) release in CA3 induced by chronic stress is responsible, and glucocorticoids have a permissive role and act synergistically with EAAs in producing neuronal damage. Moreover, glucocorticoids increase synapsin I, which has a key role in the release of neurotransmitter, including EAAs. Hereby, we hypothesize that major depression involves synapsin I alteration and that mifepristone blocks this alteration. In the present study, we observed both the expression of hippocampal synapsin I and depression-associated behavior in a rat model of depression induced by chronic unpredictable mild stress (CUMS). The result showed that a region-dependent synapsin I alteration occurs in the rat hippocampus after 21 days of CUMS, that is, it increases in dentate gyrus (DG)/CA3 and decreases in the CA1 region. Correlation analysis indicated that the decrease of synapsin I in CA1 is highly correlated with the increase in the DG/CA3 subfield. Simultaneously, the region-dependent alteration of synapsin I is correlated with depression-associated behaviors. Both the alteration of synapsin I and the depression-associated behavior were rapidly restored after treatment with mifepristone for 1 week. The result suggests that the molecular mechanism underlying the treatment of depression with mifepristone is associated with the rapid repair of the synaptic alteration.

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“…These modifications of neuronal function most likely require the transcription of new molecules. Studies show that antidepressants, which primarily enhance 5-HT levels in the synapse also affect transcription of a number of genes including synapse-associated proteins and neuropeptides (Alfonso et al, 2005;Yamada and Higuchi, 2005;Holmes et al, 2006;Iwata et al, 2006;Sairanen et al, 2007). Furthermore, chronic antidepressant treatment upregulates the transcription factor cAMP response element binding protein (CREB) (Nibuya et al, 1996;Sairanen et al, 2005) and overexpression of CREB is sufficient to induce antidepressant-like effects in animal models of depression (Wallace et al, 2004), indicating the importance of transcription for antidepressant actions.…”

Section: Introductionmentioning

confidence: 99%

The Neuropeptide VGF Produces Antidepressant-Like Behavioral Effects and Enhances Proliferation in the Hippocampus

Krol²,

et al. 2007

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Brain-derived neurotrophic factor (BDNF) is upregulated in the hippocampus by antidepressant treatments, and BDNF produces antidepressant-like effects in behavioral models of depression. In our previous work, we identified genes induced by BDNF and defined their specific roles in hippocampal neuronal development and plasticity. To identify genes downstream of BDNF that may play roles in psychiatric disorders, we examined a subset of BDNF-induced genes also regulated by 5-HT (serotonin), which includes the neuropeptide VGF (nonacronymic). To explore the function of VGF in depression, we first investigated the expression of the neuropeptide in animal models of depression. VGF was downregulated in the hippocampus after both the learned helplessness and forced swim test (FST) paradigms. Conversely, VGF infusion in the hippocampus of mice subjected to FST reduced the time spent immobile for up to 6 d, thus demonstrating a novel role for VGF as an antidepressant-like agent. Recent evidence indicates that chronic treatment of rodents with antidepressants increases neurogenesis in the adult dentate gyrus and that neurogenesis is required for the behavioral effects of antidepressants. Our studies using

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Hippocampal synapsin I, growth-associated protein-43, and microtubule-associated protein-2 immunoreactivity in learned helplessness rats and antidepressant-treated rats

Cited by 50 publications

References 70 publications

Effects of Repeated Citalopram Treatments on Chronic Mild Stress-Induced Growth Associated Protein-43 mRNA Expression in Rat Hippocampus

Effects of Repeated Citalopram Treatments on Chronic Mild Stress-Induced Growth Associated Protein-43 mRNA Expression in Rat Hippocampus

Mifepristone Repairs Region-Dependent Alteration of Synapsin I in Hippocampus in Rat Model of Depression

The Neuropeptide VGF Produces Antidepressant-Like Behavioral Effects and Enhances Proliferation in the Hippocampus

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