Kainic acid-induced seizures in rats represent an established animal model for human temporal lobe epilepsy. The neuropathological sequelae include acute status epilepticus followed by neurodegeneration in the CA1 and CA3 sector of the Ammon's horn and of interneurons in the hilus of the dentate gyrus. After about three weeks spontaneous recurrent seizures become manifest. We investigated changes in messenger RNA expression of 13 GABA_A receptor subunits in the hippocampus of rats in the initial phase (6h, 12h and 24h) after acute kainic acid-induced status epilepticus and seizure-related neuronal cell damage during and after acquisition of spontaneous recurrent seizures (seven and 30 days after kainic acid injection). In the granule cell layer, initial (after 6 to 12h) decreases in (α₂, α₃, α₅, β₁, β₃, γ₂ and δ messenger RNAs (by about 25 to 50%) were accompanied by increases (by about 50%) in α₁, α₄, and β₂ messages. At later intervals (after seven to 30 days), expression of α₂, α₄, β₃ and γ₂ messenger RNAs recovered to control values, with α₅ and δ messenger RNA still being reduced (by 15 and 40% below control levels, respectively). Concentrations of the transcripts encoding for α₁, α₃, β₁, β₂, became markedly enhanced (between 20 and 50% of controls). Within the pyramidal cell layers CA1 and CA3, decreases in α₂, α₄, α₅, β_1–3 and γ₂ messenger RNAs were detected after seven to 30 days, reflecting pronounced neurodegeneration in these areas. The α₁ transcript was decreased in CA3 after 24h and increased to control levels indicating compensatory up-regulation of this message after seven days. Messenger RNAs encoding for α₃-, γ₁-, and γ₃-subunits were detected at rather low levels, α₆ was not present in the hippocampus. Our data suggest a fast but transient change in the expression of messenger RNAs encoding for different subunits of the GABA_A receptor in the granule cell layer of the dentate gyrus. This is followed by a lasting augmentation of messenger RNAs encoding different GABA_A receptor subunits in the same cell layer indicating long-lasting GABAergic inhibition. Changes within the pyramidal cell layer are mostly determined by concomitant neurodegenerative processes.