Limbic encephalitis is an adaptive autoimmune disease, induced by different autoantibodies, which target extracellular neuronal epitopes, such as NMDA or GABAB receptors1,2. Recently our group found another human antibody, which binds to the α1 subunit of the GABAA receptor. Since the GABAA receptor is responsible for the majority of fast inhibitory neurotransmission, we investigated changes in GABAergic activity and the excitability in brain regions containing the α1 subunit. Therefore, we performed a functional in-vitro characterization by incubating acute brain slices with the antibody and performing electrophysiological recordings in the somatosensory cortex (S1). The single-cell analysis of pyramidal neurons in S1 showed a significantly reduced frequency of GABAergic events. In contrast examining the excitability by counting the number of action potentials generated in response to a current step, showed no effect of the antibody. By using transgenic GFP-GAD-65 mice we separately explored the antibody’s effects in interneurons only. There, we found a non-significant difference in the amplitude of GABAergic events, but no changes in the frequency. Fluorescence staining confirmed the specificity of the antibody binding in S1 and hippocampal regions. In conclusion, the antibody seems to cause an increased excitability especially in pyramidal cortical neurons mediated by a reduced GABAergic activity.