• Journal of Ginseng Research
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• 제33권1호
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• pp.48-54
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• 2009

Epileptifrom discharges were induced in the telencephalon of the adult zebrafish via perfusion with pentylenetetrazole (PTZ), bicuculline methiodide, kainic acid-treated artificial cerebrospinal fluid (aCSF), and $Mg^{2+}$-free aCSF. Ginseng total saponin [GTS ($50{\mu}g/ml$)] was shown to attenuate the occurrence rate of epilpetiform discharges by 50-75%, compared to the control. Ginsenoside $Rg_1$ ($130{\mu}M$) reduced the epileptiform discharges in the isolated telencephalon and delayed the occurrence of behavioral seizures observed from the adult zebrafish placed in the PTZ (10 mM)-containing aquarium water. However, Re was not effective in the suppression of epileptiform discharges and behavioral seizures. These results indicate that $Rg_1$ may be useful in the control of epileptiform discharges and effective in controlling behavioral seizures, and that the zebrafish can be used as a model animal for the testing of potential anticonvulsant drugs.

• Molecules and Cells
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• 제43권1호
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• pp.76-85
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• 2020

MARCH5 is a RING finger E3 ligase involved in mitochondrial integrity, cellular protein homeostasis, and the regulation of mitochondrial fusion and fission. To determine the function of MARCH5 during development, we assessed transcript expression in zebrafish embryos. We found that march5 transcripts were of maternal origin and evenly distributed at the 1-cell stage, except for the mid-blastula transition, with expression predominantly in the developing central nervous system at later stages of embryogenesis. Overexpression of march5 impaired convergent extension movement during gastrulation, resulting in reduced patterning along the dorsoventral axis and alterations in the ventral cell types. Overexpression and knockdown of march5 disrupted the organization of the developing telencephalon and diencephalon. Lastly, we found that the transcription of march5 was tightly regulated by the transcriptional regulators CHOP, C/EBPα, Staf, Znf143a, and Znf76. These results demonstrate the essential role of March5 in the development of zebrafish embryos.

• Animal cells and systems
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• 제13권4호
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• pp.411-418
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• 2009

We are reporting the identification, expression patterns, and possible biological functions of zebrafish kif3b (kif3bz) encoding 475 amino acids. Kif3Bz contains the kinesin motor domain, catalytic domain, KISc domain, and one single coiled coil domain. Phylogenetic analysis indicates that kif3bz is a highly conserved gene among the tested vertebrates. First of all, both maternal and zygotic messages of kif3bz were evenly distributed in the blastomeres at 2-cell stage. Its ubiquitous expression throughout the blastomeres continued till 40% epiboly. However, kif3bz transcripts became restricted in Kupffer's vesicle at tailbud and 6-somite stages. At 13-somite stage, kif3bz expression pattern became specific to the telencephalon, diencephalon, trigeminal placode, and somites. Such expression patterns were further intensified in the telencephalon, diencephalons, hind brain, pronephric ducts, optic vesicles, and spinal cord neurons in the 23-somite stage embryos, and last till 24 hpf. We discussed possible functions of Kif3Bz related to the vertebrate embryonic development.

• 생물정신의학
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• 제30권1호
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• pp.17-23
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• 2023

Objectives This study aims to develop valid experimental models for depression through chronic reserpine exposure to zebrafish (Danio rerio). Methods The effect of chronic reserpine on zebrafish behavior in the novel tank was examined. Changes of gene expression on telencephalon were also investigated. Results Chronic reserpine (40 mg/L, 7 days) induced overt behavioral effects, but markedly reduced activity, resembling motor retardation in depression. In telencephalon of zebrafish, gene expression associated with monoamine oxidase and norepinephrine transporter was decreased. Expression of serotonin transporter gene was increased. Conclusions Our results show that the pharmacological model of depression in zebrafish can induce not only behavioral changes, but also monoamine changes in the homology of human mood regulation centers.