abstract
- Double-pulse stimulation of the perforant path input to the dentate gyrus was used in the following experiments to produce paired pulse depression in that site. This effect provided an estimate of GABA-mediated recurrent inhibition. The depression was enhanced by drugs that facilitate or mimic GABA action and attenuated by drugs which block GABA transmission. Paired-pulse depression was significantly increased following amygdala kindling and was further enhanced to near maximal levels by subsequent kindling in the dentate. In addition, kindling did not increase the rate at which inhibition failed under conditions of excessive activation. Trains of 5 Hz stimulation, applied to the perforant path, caused paired-pulse depression to disappear and elicited a brief AD. Following kindling, the latency to AD onset tended to be increased rather than shortened, suggesting an enhanced resistance to inhibitory failure. These results indicated that kindling increased, rather than reduced, inhibition in the dentate gyrus.