Lack of tau expression modifies epileptogenesis associated neuroplasticity in the ventral dentate gyrus in a mouse model of temporal lobe epilepsy
Deletion of the microtubule-associated protein, tau reduces seizure burden in rodent models of genetic epilepsies and suppresses evoked seizures. In the intrahippocampal kainate (IHK) model of acquired temporal lobe epilepsy (TLE), mice lacking tau expression develop spontaneous seizures, but at a lower rate than controls. Mechanisms by which tau deletion modifies the development of acquired TLE…
A study of a mouse model of temporal lobe epilepsy reveals that the absence of tau protein alters the neuroplasticity involved in the progression of epilepsy. In these mice, the development of seizures results in heightened firing of action potentials in the ventral dentate granule cells, which are located away from the initial focal injury.
The absence of tau also leads to an increase in inhibitory synaptic input to these cells, both on the same side and the opposite side of the lesion. This was demonstrated through optogenetic stimulation of interneurons in the mice, which showed an increase in inhibitory synaptic activity in the ventral dentate gyrus once epilepsy had taken hold.
These findings suggest that tau expression plays a role in suppressing inhibitory synaptic reorganization in the dentate gyrus, and its absence may contribute to the altered seizure expression seen in this model of epilepsy.
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