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Ornithine decarboxylase is differentially induced by kainic acid during brain development in the rat
Affiliation:1. Department of Pediatrics, St. Mary’s Hospital, Fukuoka, Japan;2. Department of Pediatrics and Child Health, Kurume University School of Medicine, Fukuoka, Japan;3. Center for Bio-Statistics, Kurume University School of Medicine, Fukuoka, Japan;1. Department of Pediatrics, Sapporo Medical University School of Medicine, Sapporo, 060-8556, Japan;2. Department of Neural Regenerative Medicine, Research Institute for Frontier Medicine, Sapporo Medical University School of Medicine, Sapporo, 060-8556, Japan;3. Department of Neurology, Yale University School of Medicine, New Haven, CT, 06510, USA;4. Center for Neuroscience and Regeneration Research, VA Connecticut Healthcare System, West Haven, CT, 06516, USA;1. Department of Clinical Pharmacy, Jagiellonian University Medical College, 9 Medyczna Street, 30-688 Krakow, Poland;2. Department of Radioligands, Jagiellonian University Medical College, 9 Medyczna Street, 30-688 Krakow, Poland;1. Department of Cell Processing and Transfusion, The Institute of Medical Science, The University of Tokyo, Tokyo, Japan;2. Department of Obstetrics, NTT Medical Center Tokyo Hospital, Tokyo, Japan;3. Division of Molecular Therapy, Center for Advanced Medical Research, The Institute of Medical Science, The University of Tokyo, Tokyo, Japan
Abstract:
The induction of brain ornithine decarboxylase (ODC) as a consequence of systemic kainic acid administration was studied in the hippocampus and the olfactory cortex-amygdala area of 10-day-old rat pups and 30-day-old young rats. In pups, ODC levels were moderately increased (plus 50–80%) 4 h after kainic acid administration, coming back quickly to control levels afterwards. In young rats, instead, ODC levels were dramatically increased by 17–25-fold, 16 h after kainic acid administration and decreased towards basal levels 48–72 h after injection. The present results suggest that the process of excitotoxic ODC induction can be split in two phases: a first phase characterized by moderate induction and essentially linked to the overstimulation of brain circuits and a second phase, during which a dramatic enzyme stimulation is accompanied by the appearance of neurodegenerative pathology.
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