Possibilities and limits of EEG analysis in mouse models for epilepsy

H.E. Krestel

Pharmacology and Toxicology, University Zurich, Zurich, Switzerland

My talk will discuss possibilities and limits of one and two channel EEG recordings and their analysis, exemplified by presenting data of the following mouse models for epilepsy. The first mouse model carries a point mutation in the channel pore of AMPA-type glutamate receptors (GluRs) that mediate the majority of fast excitatory synaptic transmission in the brain. These mice show myoclonic seizures, temporal lobe epilepsy and characteristic interictal activity. The second mouse model contains a point mutation in the ligand binding domain of GABA receptors that comprise the majority of fast inhibitory neurotransmission. This point mutation was first described in a family with absence epilepsy and subsequently introduced into mice. However, genetically modified mice showed myoclonic jerks, comparable to mice with the GluR point mutation, but no tonic-clonic seizure attacks.

Third, mice deficient for a receptor subunit (GBR2) of GABA-B receptors that mediate slow inhibitory neurotransmission showed generalized tonic-clonic attacks without myoclonic jerks. EEG patterns and behaviour of seizure attacks started and ended abruptly and interictal EEG showed predominantly polyspike activity (manuscript in preparation). No human epilepsy with a defect GBR2 subunit is known to date.

Technical and methodological possibilities and limits will be discussed by data interpretation between these mouse models.

Paper presented at Measuring Behavior 2005 , 5^th International Conference on Methods and Techniques in Behavioral Research, 30 August - 2 September 2005, Wageningen, The Netherlands.

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