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GABA-gated chloride ion influx and receptor binding studies in C57BL6J and DBA2J mice |
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| Authors: | Onnfoh Yu Masatoshi Ito Ted H. Chiu Howard C. Rosenberg |
| Affiliation: | 1. Department of Neuroscience, Tufts University School of Medicine, 136 Harrison Avenue, Boston, MA 02111, USA;2. Cell Signal Unit, Okinawa Institute of Science and Technology Graduate University, Okinawa 904-0495, Japan;3. Discovery Biology, Discovery Sciences, R&D, AstraZeneca, Boston, MA, USA;4. Department for Biochemistry and Biomedicine, University of Sussex Brighton, Brighton BN1 9RH, UK;5. Department of Neuroscience, Physiology and Pharmacology, University College London, London WC1 6BT, UK;1. Faculty of Biological and Environmental Sciences, Molecular and Integrative Biosciences, University of Helsinki, Helsinki, Finland;2. Neuroscience Center (HiLIFE), University of Helsinki, Helsinki, Finland |
| Abstract: | GABA-gated chloride ion influx was measured in brain 'microsac' preparations of young (20-22-day-old) and older (40-42-day-old) C57BL6J and DBA2J mice. The young DBA2J mice are susceptible to audiogenic seizures. GABA sensitivity was reduced in young DBA2J mice as compared to age-matched C57BL6J mice or older mice of either strain. Age and strain differences in ligand binding to GABA/benzodiazepine receptor complex and glutamate receptor could not account for this finding. These results provide evidence for a defect in GABA-gated chloride ion influx in audiogenic seizure-susceptible DBA2J mice. |
| Keywords: | Audiogenic seizure Chloride ion Age γ -Aminobutyric acid (GABA) receptor Benzodiazepine receptor Glutamate receptor Mouse |
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