29-30 January, 2020 - Szeged, Hungary


Abstract details



Júlis Baross11, Zsolt Kovács2, Péter Papp3, Péter Szocsics1, Zsófia Maglóczky1

1 Human Brain Research Laboratory, Institute of Experimental Medicine, Hungarian Academy of Sciences, Budapest, 1083, Hungary

2 Savaria Department of Biology, Savaria University Centre, ELTE Eötvös Loránd University, Szombathely, 9700, Hungary

3 Laboratory of Cerebral Cortex Research, Department of Cellular and Network Neurobiology, Institute of Experimental Medicine, Hungarian Academy of Sciences, Budapest, 1083, Hungary

We have investigated if there is a relationship between the onset of absence seizures and the loss of inhibitory interneurons in cortical and hippocampal regions, observed in a previous study, using the WAG/Rij rat strain, an animal model of absence epilepsy. Absence seizures in the WAG/Rij rat strain emerge from 2-3 months of age, originating from the somatosensory cortex, and are associated with alterations of the inhibitory-excitatory network of thalamic and cortical regions. However, it is unclear whether seizures might emerge as a result of an originally lower interneuron density in young, pre-epileptic rats, or seizures itself are responsible for the interneuron loss observed in older, seizing rats. Thus, interneuron densities in calretinin (CR)- and parvalbumin (PV)-immunostained sections of the hippocampus and the somatosensory cortex were compared across 6-week-old, pre-epileptic and 8-month-old, epileptic WAG/Rij, and seizure-free, age-matched WISTAR rat strains. It was found that pre-epileptic WAG/Rij rats show a decreased density of PV-immunolabeled interneurons in the infragranular layer of the somatosensory cortex. However, control-like cell density was found in case of the supra- and granular layers, although cell density significantly decreased after the onset of seizures, by 8 months of age. Based on the results, it seems that the originally lower density of PV-immunolabeled cells in the infragranular layer of the somatosensory cortex might be one of the factors involved in the generation of absence seizures, which might lead to the further loss of interneurons in other layers of the somatosensory cortex, observed at 8 months of age. Support: National Research, Development and Innovation Office of Hungary (grant K 125436) and National Brain Research Program (2017-1.2.1-NKP-2017-00002)