The G-protein coupled receptor GABAB is an important regulator of presynaptic neurotransmitter release and postsynaptic excitability. In anti-GABABR autoimmune encephalitis pathogenic autoantibodies (aAB) target the GABAB receptor, leading to various symptoms, including epilepsy, cognitive disorders, and short-term memory loss. Here we aimed at evaluating the influence of these aAB on hippocampal-dependent cognitive and epileptic pathways. We used purified patient-derived antibodies (control- and anti-GABABR-IgG) in a chronic mouse model of the disease to evaluate the memory formation via Novel Object Recognition test. Ex-vivo recordings of field potentials and the long-term potentiation (LTP) paradigm were performed to evaluate the synaptic plasticity in CA1. In-vivo EEG recordings in a mouse model of acute PTZ induced epilepsy was used to evaluate the anti-GABABR-IgG influence on seizure onset and severity. Moreover, super resolution microscopy was applied in primary neurons to elucidate preferential IgG binding sites and structural changes in synapses. Evaluation of cognitive function suggests an influence of the anti-GABABR-IgG on the consolidation and maintenance of contextual memory. These findings are supported by the field potentials analysis, which revealed a disturbed LTP induction and an alteration on the network excitability. Super resolution imaging gave further insights on anti-GABABR-IgG influence on peri-synaptic structure and receptors localization.Preliminary in-vivo EEG data have been collected, and simultaneous behavioral evaluation of epileptic seizures suggest a proconvulsive effect mediated by the anti-GABABR-IgG.Our results provide insight on the pathophysiology mediated by patient derived anti-GABABR-IgG, elucidating potential mechanism involved in cognitive impairment and seizure susceptibility in this subtype of autoimmune encephalitis.