Evoked epileptiform discharges in the rat anterior piriform cortex: generation and local propagation

The purpose of this study was to identify cellular and synaptic properties of neurons in a small region within the anterior piriform cortex (aPC), ter med the area tempestas (AT), responsible for triggering forebrain seizures in rats. Using a brain slice preparation, we performed whole-cell patch rec ordings from neurons in the regions overlapping the functionally defined AT . Local electrical stimulation activated synaptic inputs to neurons in thes e regions, collectively termed the deep aPC (daPC). Synaptic inputs were bl ocked by selective ionotropic glutamate receptor antagonists. Excitatory bu rsts were evoked from 59% of daPC neurons as the stimulus intensity was rai sed above a precise threshold. Secondary bursts (6-15 Hz) occurred in 34% o f daPC neurons. Evoked bursts were synaptically driven, as they were blocke d by TTX (1 mu M) or 2,3-dihydroxy-6-nitro-7-sulfamoyl-benzo( f)quinoxaline (NBQX, 1 mu M), but not by inclusion of cesium and N-(2,6-dimethylphenylca rbamoylmethyl) triethylammonium (QX-314) in the internal patch solution. Ne ither augmentation of excitatory nor suppression of inhibitory transmission were required to evoke bursts from daPC neurons. However, bicuculline (20 mu M) lowered the threshold intensity for evoking discharges and increased the incidence and duration of evoked bursts, indicating active inhibitory c ontrol of daPC neurons. Stimulation in the daPC evoked epileptiform field p otentials from layer II of the adjacent PC and bursts from layer II pyramid al neurons. This work demonstrates that synaptically dependent excitatory b urst discharges can be evoked from daPC neurons without altering the balanc e between synaptic excitation and inhibition. Stimuli that trigger bursts i n daPC neurons also generate epileptiform activity in layer II pyramidal ce lls, indicating that propagation of excitatory activity triggered from the daPC to the pyramidal neurons of the aPC can contribute to the initiation o f seizures induced by disinhibition of the AT in vivo. (C) 2000 Elsevier Sc ience B.V. All rights reserved.