Positive titers for glutamic acid decarboxylase (GAD) antibodies have been reported in a variety of neurological disorders such as stiff-person syndrome, sporadic ataxia and some cases of epilepsy. As their target is a cytoplasmic enzyme, the pathogenic role of GAD-antibodies is still under debate. Here we have tested the GABAergic transmission in the CA1-region of hippocampal slices after stereotactic injection of human cerebrospinal fluid samples in order to reveal functional consequences on the synaptic level. First, in a model of acute epileptiform activity in extracellular field-recordings we could show an enhancement of recurrent epileptic discharges in slices from GAD-antibody treated animals. However, intracellular recordings with sharp microelectrodes from CA1-neurons failed to detect amplitude changes on GABA-mediated IPSPs. Patch clamp recordings of these cells confirmed our results and in addition indicated that kinetic changes could also not be observed. While stereotactic injection of GAD-antibodies did exert a proepileptogenic effect on in vitro slices, GABAergic synaptic transmission appeared to be intact in these tissues.