Kindling and Plasticity of the Hippocampal Inhibitory System

Abstract

<p>Kindling involves the repeated application of epileptogenic stimulation to certain brain sites until fully generalized behavioral convulsions occur. Input/output relationships (determined by recording responses evoked at different stimulation intensities) and paired-pulse facilitation/depression effects were monitored in the hilus of the hippocampal dentate gyrus as stimulation pulses were applied to the perforant path. These effects were measured before, during and after kindling the perforant path or the hilus of the dentate gyrus.</p> <p>After kindling was completed, the perforant path-kindled animals showed an increase in population spike height (related to the number of cells firing) at the higher intensities but a decrease at lower intensities. A small increase in the slope of the rising phase of the population EPSP was observed at the higher intensities. The dentate gyrus-kindled animals showed a progressive decrease in population spike height during kindling, while the slope increased in magnitude. All of these kindling-induced effects, except for the increase in slope, appeared to decay towards pre-kindling levels over a 4 week stimulation-free period after the completion of kindling.</p> <p>Paired-pulse depression of the population spike height was "potentiated" in both groups as a result of kindling. Paired-pulse effects returned towards pre-kindling levels over a 4 week stimulation-free period post-kindling. This decay was especially clear in the perforant path-kindled group.</p> <p>Kindling the perforant path resulted in a significant increase in number of benzodiazepine receptors. This increase in receptor number is believed to underly the kindling-induced increase in paired-pulse depression. Results indicated that the increase in receptor number may decline with time after kindling is terminated.</p> <p>It was concluded that almost all kindling-induced effects studied disappear over time after kindling is terminated. They are dependent on the occurrence of epileptogenic stimulation. Characteristics of potentiation of the hippocampal inhibitory system appear to be similar to those of potentiation of the hippocampal excitatory system.</p>