Dynamic Pattern of Gene Expression of ZnT-4, Caspase-3, LC3, and PRG-3 in Rat Cerebral Cortex Following Flurothyl-Induced Recurrent Neonatal Seizures |
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Authors: | Hong Ni Xing Feng Zhuo-jun Xiao Lu-yang Tao Mei-fang Jin |
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Institution: | (1) Neurology Laboratory, Soochow University Affiliated Children’s Hospital, No. 303, Jingde Road, Suzhou, 215003, People’s Republic of China;(2) Institute of Neuroscience, Soochow University, Suzhou, 215003, People’s Republic of China |
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Abstract: | Zinc transporters, plasticity-related genes, and autophagic/apoptotic pathway both are associated with developmental seizure-induced
brain excitotoxicity. Here, for the first time, we report the timing of expression pattern of zinc transporter 4 (ZnT-4),
plasticity-related gene 3 (PRG-3), specific marker of autophagic vacuoles (LC3), and apoptotic marker caspase-3 in cerebral
cortex following neonatal seizures. A seizure was induced by inhalant flurothyl daily in neonatal Sprague–Dawley rats from
postnatal day 6 (P6). Rats were assigned into the recurrent-seizure group (RS, seizures induced in six consecutive days) and
the control group. At 1.5 h, 3 h, 6 h, 12 h, 24 h, 48 h, 7 days, and 14 days after the last seizure, the mRNA level of the
four genes in cerebral cortex was detected using RT–PCR method. At an early period 6 h or 12 h after the last seizures, both
ZnT-4 and LC3 showed significantly up-regulated mRNA level while PRG-3 showed significantly down-regulated mRNA level at 12 h
in cerebral cortex of RS group than those at the corresponding time point in control group. In the long-term time point of
7 days after the last seizure, the mRNA level of caspase-3 down-regulated; meanwhile, there was up-regulated mRNA level of
LC-3 in RS group when compared to the control rats. This is the first report investigating the gene expression pattern of
ZnT-4, PRG-3, LC-3, and caspase-3 in the developing brain. The results suggest that the disturbed expression pattern of the
four genes might play a role in the pathophysiology of recurrent neonatal seizure-induced acute and long-term brain damage. |
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