Effects of projected cortical epileptiform discharges on neuronal activities in cat VPL. I. Interictal discharge

Recordings were made from 182 cells in n. ventralis postero lateralis (VPL) of the cat during penicillin induced interictal epileptiform discharges in the somatosensory cortex. Interictal cortical discharges generated high frequency bursts of impulses in corticothalamic axons which project focally to the functionally related zone of VPL. The projected discharges produce a prominent inhibition of thalamocortical relay (TCR) cells which is presumably mediated through thalamic inhibitory interneurons. Epilepsy evoked inhibitory postsynaptic potentials (IPSPs) contribute to a depression in conduction of sensory volleys through VPL. Initial excitatory synaptic effects of interictal discharges were recorded in 42% of neurons which were not antidromically invaded following cortical stimulation. A proportion of these cells presumably represent thalamic inhibitory interneurons activated by corticothalamic axons. Only 11% of TCR cells showed initial excitation during projected discharges. Since TCR neurons in VPL normally provide a powerful specific afferent projection to the focus, inhibition of their activities would produce a partial functional deafferentation of the epileptic neuronal aggregate. This negative feedback may serve to limit the frequency of repetitive interictal discharges and the transition to the ictal episode. The efficacy of this mechanism is limited by the generation of bursts of spikes in thalamocortical axons. Antidromic bursts of spikes originating in intracortical axons invaded the cell bodies of 36 of 61 identified TCR cells. These bursts had a latency of about 30 ms from the onset of the cortical epileptiform event, and fell in the midst of the epilepsy evoked IPSP. Antidromic bursts are presumably initiated by nonsynaptic depolarization of TCR axons and may be an important mechanism for generation of synchronous intense excitation in cells of the epileptogenic focus.