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  • Title: GABAergic neurotransmission in the C57BL/10 sps/sps mouse mutant: a model of absence seizures.
    Author: Ortiz JG, Negrón AE, Thomas AP, Heimer H, Moreira JA, Cordero ML, Aranda J, Bruno MS.
    Journal: Exp Neurol; 1991 Sep; 113(3):338-43. PubMed ID: 1655511.
    Abstract:
    The C57BL/10 sps/sps mouse mutant displays generalized absence seizure-like behavior. In these mice, glutamic acid decarboxylase activity is reduced in the cortex and hippocampus. Tritiated flunitrazepam binding (3H-flu) is reduced in these areas, as well as in midbrain, cerebellum, and pons-medulla. Quantitative [3H]-flunitrazepam binding autoradiography confirms these observations. GABA uptake by synaptosomes from sps/sps mice is also reduced in all the areas studied. Potassium-stimulated, Ca(2+)-dependent release of radioactivity from synaptosomes preloaded with [14C]-GABA is reduced in the hippocampus, increased in midbrain and pons-medulla, but remains unaltered in the cortex. These results suggest region-specific alterations in GABAergic neurotransmission that may be responsible for the absence-like seizures in C57BL/10 sps/sps mice.
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