title: Decrease in hippocampal [3H]vinylidene kainic acid binding in genetically epilepsy-prone rats.
abstract: Specific [3H]vinylidene kainic acid binding to the kainate-sensitive subtype of glutamate receptor was studied in brain of 31-day-old non-epileptic Sprague-Dawley control and two colonies of genetically epilepsy-prone rats using in vitro autoradiographic techniques. At 37.5 nM [3H]vinylidene kainic acid, specific [3H]vinylidene kainic acid binding was reduced significantly by 18 and 22% in dorsal and ventral hippocampal formation stratum lucidum of 31-day-old genetically epilepsy-prone-9 rats compared with non-epileptic controls. Hippocampal [3H]vinylidene kainic acid binding was reduced in genetically epilepsy-prone-3 rats by 15 and 18%, but these reductions were not statistically significant. Saturation of [3H]vinylidene kainic acid binding studies indicated that the total number of ventral hippocampal [3H]vinylidene kainic acid binding sites was decreased by 21% in genetically epilepsy-prone-3 rats and 28% in genetically epilepsy-prone-9 rats. The reduction in ventral hippocampal [3H]vinylidene kainic acid binding in genetically epilepsy-prone rats resembles the reduction in ventral hippocampal [3H]vinylidene kainic acid binding sites observed in perinatal hypothyroid rats. As genetically epilepsy-prone rats are hypothyroid during the neonatal period, the reduction in hippocampal [3H]vinylidene kainic acid binding in the genetically epilepsy-prone rats may be a consequence of a hypothyroid-induced defect in the development or maturation of the hippocampal mossy fiber projection in genetically epilepsy-prone rats. An alternative hypothesis is that the putative occurrence of spontaneous limbic seizures in genetically epilepsy-prone rats may lead secondarily to a reduction in hippocampal [3H]vinylidene kainic acid binding sites.
authors.affiliation: Department of Pharmacology, University of New Mexico School of Medicine, Albuquerque 87131.
authors.forename: S A
authors.initials: SA
authors.lastname: Mills
authors.forename: S
authors.initials: S
authors.lastname: Razani-Boroujerdi
authors.forename: C E
authors.initials: CE
authors.lastname: Reigel
authors.forename: P C
authors.initials: PC
authors.lastname: Jobe
authors.forename: D D
authors.initials: DD
authors.lastname: Savage
mesh_terms: D000818:Animals; D001345:Autoradiography; D004827:Epilepsy / Q000235:genetics / Q000378:metabolism*; D005971:Glutamates / Q000378:metabolism; D006624:Hippocampus / Q000378:metabolism*; D007608:Kainic Acid / Q000378:metabolism*; D007700:Kinetics; D009928:Organ Specificity; D051381:Rats; D011919:Rats, Inbred Strains; D017470:Receptors, Glutamate; D017981:Receptors, Neurotransmitter / Q000378:metabolism*; D012016:Reference Values; D014316:Tritium
chemical_list: D005971:Glutamates; D017470:Receptors, Glutamate; D017981:Receptors, Neurotransmitter; D014316:Tritium; D007608:Kainic Acid