GABAergic neurotransmission in the C57BL/10 sps/sps mouse mutant: a model of absence seizures.
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.
Ortiz
J G
JG
Department of Pharmacology, University of Puerto Rico, School of Medicine San Juan 00936-5067.
Negrón
A E
AE
Thomas
A P
AP
Heimer
H
H
Moreira
J A
JA
Cordero
M L
ML
Aranda
J
J
Bruno
M S
MS
D000818:Animals; D001921:Brain / Q000378:metabolism*; D004832:Epilepsy, Absence / Q000378:metabolism*; D051379:Mice; D008817:Mice, Mutant Strains / Q000378:metabolism*; D009435:Synaptic Transmission; D005680:gamma-Aminobutyric Acid / Q000378:metabolism*
D005680:gamma-Aminobutyric Acid