Abstract
The linkage-testing strain of ABP Le mice carries six mutations which express in easily identifiable phenotypes. By crossing this strain with a traditional inbred strain ( C57BL 6ByJ ) which is the ‘wild type’ for the mutated ABP Le loci, we produced Mendelian populations, intercrosses and backcrosses so as to estimate whether the sensitivity to methyl β-carboline-3-carboxylate (β-CCM), a benzodiazepine receptor inverse agonist, and anxiety-related behaviour could be related to a common genetically determined substrate. We have shown that one locus on chromosome 9 is associated with β-CCM-induced seizures and three loci on chromosomes 4, 7 and 9 are associated with anxiogenic processes. Analysis of [ 3H]flumazenil binding suggested a possible involvement of a B max decrease in both β-CCM-induced seizures and anxiogenic processes. The putative common genetic regulation of both mechanisms is discussed.
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