Behavioral Evidence for Cognitive Dysfunctions in the (BALB/cByJ-Kv1.1mceph/mceph) Mouse Model for Epilepsy
نویسندگان
چکیده
The epileptic mouse model BALB/cByJ-Kv1.1 (mceph/mceph) is homozygous for a spontaneous mutation truncating the Shaker-like voltage gated potassium channel, Kv1.1 (Kcna1). The mceph/mceph mice are asymptomatic at birth, but develop from 3 weeks of age epileptic seizures, overgrowth and neuronal hyperplasia of the hippocampus. Hippocampal cognitive function of the mice was examined by investigating emotional memory using the aversive Passive Avoidance (PA) task combined with studies of explorative behavior using the non-aversive Novel Cage test (NCT). The behavioural results were examined by multivariate analysis. Compared to wild type and heterozygous mice, the mceph/mceph mice displayed lower exploratory and safety assessment behavior in the NCT and impairment in PA retention 24 hours after training, indicating an impairment in cognitive functions. In conclusion, the epileptic mouse model BALB/cByJKv1.1mceph/mceph, with chronic epilepsy related to potassium-channelopathy, display a behavioural phenotype characterized by impairments in emotional memory and defensive motivational responses probably related to hippocampal dysfunctions.
منابع مشابه
Extramural Update December 2003
Background: Mutations in the Shaker-like voltage-gated potassium channel Kv1.1 are known to cause episodic ataxia type 1 and temporal lobe epilepsy. Mice that express a malfunctional, truncated Kv1.1 (BALB/cByJ-Kv1.1mceph/mceph) show a markedly enlarged hippocampus and ventral cortex in adulthood. Results: To determine if mice lacking Kv1.1 also develop a brain enlargement similar to mceph/ mce...
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