In order to identify lasting alterations in gamma-aminobutyric acid (GABA) neurons in the kindling model of epilepsy, immunocytochemical techniques were used to quantify the number of GABA-immunoreactive (IR) neurons in different regions of the hippocampal formation (HCF) of amygdala-kindled rats, 40 days after the last fully kindled seizure. A new, highly specific monoclonal GABA antibody was used for these experiments. Unexpectedly, the antibody not only stained neurons in CA1, CA3, and hilus, but also intensively stained granule cells (GCs) in the dentate gyrus (DG) of both kindled rats and non-kindled controls, indicating that GCs may be capable of synthesizing GABA. Comparison with a polyclonal GABA and a glutamate decarboxylase antibody showed that staining of GCs with the monoclonal GABA antibody was much more intense. The number of GABA-IR cells that were counted in different regions of the HCF, including the DG, did not differ significantly between kindled rats and controls, which does not support the hypothesis of loss of hippocampal GABAergic neurons to explain the permanency of kindled epileptogenesis.