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자료유형
학술저널
저자정보
Kim, Yeon-Hwa (Department of Biological Sciences, Institute of Molecular and Cellular Biology, Inha University) Lee, Yun-Kyoung (Department of Biological Sciences, Institute of Molecular and Cellular Biology, Inha University) Lee, Han-Sol (Department of Biological Sciences, Institute of Molecular and Cellular Biology, Inha University) Jung, Min-Whan (Neuroscience Laboratory, Institute for Medical Sciences, Ajou University School of Medicine) Lee, Chang-Joong (Department of Biological Sciences, Institute of Molecular and Cellular Biology, Inha University)
저널정보
한국통합생물학회 Animal cells and systems Animal cells and systems 제13권 제3호
발행연도
2009.1
수록면
275 - 281 (7page)

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The effects of pentylenetetrazol (PTZ), a GABA receptor antagonist, were studied on passive avoidance learning and expression of heat shock protein 70 (hsp70), neuroglobin, and fatty acid binding protein-7 (fabp-7) genes. Zebrafish were trained to stay in a dark compartment to avoid a weight dropping in an acryl shuttle box with a central sliding door. In two training sessions of 2 h interval, each consisting of 3 trials, the crossing time was significantly increased from $43.2{\pm}14.4s$ to $149.3{\pm}38.5s$ in the first training session and remained $116.1{\pm}36.0s$ s in the first trial of the second training session in the control. In zebrafish treated with PTZ before the first training session, the crossing time was significantly increased neither in the first nor in the second training session. However, the increased crossing time was maintained in the second training session when 10 mM PTZ was treated three times for 10 min at 30 min intervals between the first and second training session. Quantitative real-time PCR showed that expression level of hsp70 mRNA increased two to eight fold over that of control in the brain at 0-24 h after termination of PTZ treatment. No change in expression of neuroglobin and fabp-7 mRNA was shown in PTZ-treated zebrafish. Our studies suggest that PTZ impairs learning ability in avoidance response and also modifies expression of genes related to the neuroprotection.

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