Laminar interactions during neocortical epileptogenesis.

Interactions among laminar subpopulations of cat striate cortical neurons were assessed during the evolution of discrete and temporary epileptic foci, which were induced by selective microinjection of penicillin into different cortical layers. Field potentials and multiunit cellular discharges, evoked by selective visual field stimulation, were recorded simultaneously from 3 layers by multibarreled glass microelectrodes. Laminar response profiles at distinct stages of epileptogenesis were characterized for foci induced in superficial pyramidal, middle stellate, and deep pyramidal layers. Layer 4 was verified to be the most susceptible to epileptogenesis. Penicillin's action within this stellate layer appeared to be sufficient for epileptogenesis and was supportative of, if not necessary for, the development of foci originating in pyramidal cell layers. These findings could not be fully appreciated by monitoring only spontaneous interictal spike potentials. Of the two types of neuronal discharge routinely observed, early latency bursting was principally a characteristic of layer 4 stellate populations, whereas longer-latency bursts comparable to paroxysmal depolarization shifts were recorded equally well from both stellate and pyramidal layers. Epileptiform alterations in both field potential and unit responses were quickly evident in cortical laminae having known anatomic connections with the layer where the focus was induced: e.g. in layers 2-3 with layer 4 foci, in layers 5-6 with layers 2-3 foci, and in layer 4 with layers 5-6 foci. The spread of epileptogenesis was slower between laminae where pathways are purported to be less well developed, and appeared to be principally dependent upon the diffusion of penicillin.