|Position||Host institution||PhD enrolment||Start date||Duration|
|ESR1||P1-USAAR||Y (at USAAR)||early 2017||36 months|
Molecular and cellular mechanisms of pathological network function in mouse models of absence epilepsy
The main aim of this project is to understand how astroglial GABAB receptors contribute to healthy and pathological brain function. In particular, how the signal cascade evoked by receptor activation determines the generation and progression of seizures in absence epilepsy. For that purpose, we use a pharmacological model of absence seizures (GHB) and a genetic model in which the GABAB receptor is selectively deleted in astrocytes.
Electrophysiology of acute brain slices and in vivo imaging of Ca2+ signals using two-photon laser-scanning microscopy (2P-LSM) will be employed as well as telemetric EEG recordings and behavioural analysis. Molecular and immunohistochemical techniques will be applied to determine the extent of receptor knockout and subsequent changes in the adjacent neighbourhood.