On the ictogenic properties of the piriform cortex in vitro

We performed field potential recordings from the PC in coronal or sagittal rat brain slices along with pharmacologic manipulations of γ-aminobutyric acid (GABA)ergic and glutamatergic signaling during application of the convulsant drug 4-aminopyridine (4AP, 50 μm). Key findings: Coronal and sagittal preparations generated interictal-like and ictal-like epileptiform discharges with similar duration and frequency. Ictal-like discharges in sagittal slices were initiated mostly in the PC anterior subregion, whereas interictal activity did not have any preferential site of origin. In sagittal slices, high frequency oscillations (HFOs) at 80-200 Hz were detected mainly at the beginning of the ictal discharge in both posterior and anterior subregions. N-Methyl-d-aspartate (NMDA) receptor antagonism abolished ictal discharges, but failed to influence interictal activity. In the absence of ionotropic glutamatergic transmission, PC networks generated slow, GABA receptor-dependent events. Finally, GABA(A) receptor antagonism during application of 4AP only, abolished ictal discharges and disclosed recurrent interictal activity. Significance: Our findings demonstrate that PC networks can sustain in vitro epileptiform activity induced by 4AP. HFOs, which emerge at the onset of ictal activity, may be involved in PC ictogenesis. As reported in several cortical structures, ionotropic glutamatergic neurotransmission is necessary but not sufficient for ictal discharge generation, a process that also requires operative GABA(A) receptor-mediated signaling.

The piriform cortex (PC) is known to be epileptic-prone and it may be involved in the manifestation of limbic seizures. Herein, we have characterized some electrophysiologic and pharmacologic properties of the spontaneous epileptiform activity generated by PC networks maintained in vitro.

Our findings demonstrate that PC networks can sustain in vitro epileptiform activity induced by 4AP. HFOs, which emerge at the onset of ictal activity, may be involved in PC ictogenesis. As reported in several cortical structures, ionotropic glutamatergic neurotransmission is necessary but not sufficient for ictal discharge generation, a process that also requires operative GABA(A) receptor-mediated signaling.