Absence Seizures (AS) are sudden, non-convulsive seizures characterised by altered consciousness, behavioural arrest and 3-4 Hz spike-and-wave discharges on the ictal EEG [3]. ASs have a significant impact on the quality of life due to the risk of injury and neuropsychiatric comorbidities, such as impairments in emotional, cognitive, memory and linguistic abilities [1,5]. Moreover, cognitive impairments have been described in Genetic Absence Epilepsy Rat from Strasbourg (GAERS) rats, which is a well characterized ASs animal model [8]. Recent evidence shows that glia cell-derived neurotrophic factor (GDNF) affect GABAergic inhibitory transmission in the hippocampal network [6], and can also have a suppressing effect on spontaneous recurrent seizures in chronic animal models of epilepsy [4,7], however its seizure-suppressing mechanism is still unknown. In AS animal models, an enhancement of tonic GABAA current in the thalamus has been described due to a loss-of-function of GABA GAT1 transporter that in the thalamus is exclusively expressed in astrocytes [2]. Therefore, we are now evaluating changes of the GDNF signalling pathways in the GAERS rats. By performing western blot analysis in hippocampal tissue from GAERS rats and the respective non-epileptic control (NEC) rats we have observed a tendency of higher expression of RET, a receptor for GDNF, as well as a significant increase of the astrocyte marker, GFAP, in GAERS when compared to NEC. Our results suggest changes in the GDNF signalling pathways in ASs, that can be modulated in order to avoid the occurrence of them.