title: On the ictogenic properties of the piriform cortex in vitro.
abstract: OBJECTIVE
  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.
  
  
  METHODS
  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).
  
  
  RESULTS
  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.
  
  
  CONCLUSIONS
  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.
authors.affiliation: Montreal Neurological Institute and Department of Neurology & Neurosurgery, McGill University, Montreal, Quebec, Canada.
authors.forename: Gabriella
authors.initials: G
authors.lastname: Panuccio
authors.forename: Gonzalo
authors.initials: G
authors.lastname: Sanchez
authors.forename: Maxime
authors.initials: M
authors.lastname: Lévesque
authors.forename: Pariya
authors.initials: P
authors.lastname: Salami
authors.forename: Marco
authors.initials: M
authors.lastname: de Curtis
authors.forename: Massimo
authors.initials: M
authors.lastname: Avoli
mesh_terms: D000818:Animals; D004827:Epilepsy / Q000139:chemically induced / Q000188:drug therapy / Q000503:physiopathology*; D008297:Male; D009415:Nerve Net / Q000187:drug effects / Q000503:physiopathology*; D009833:Olfactory Pathways / Q000187:drug effects / Q000503:physiopathology*; D009924:Organ Culture Techniques; D051381:Rats; D017207:Rats, Sprague-Dawley; D011963:Receptors, GABA-A / Q000187:drug effects / Q000502:physiology*; D009435:Synaptic Transmission / Q000187:drug effects / Q000502:physiology*
chemical_list: D011963:Receptors, GABA-A