Conductance changes in neocortical propagated seizure: Seizure termination

Intracellular records were obtained from neurons located on the pericruciate gyri of cats paralyzed with gallamine triethiodide and involved in propagated seizures produced by repetitive stimulation of the homotopic contralateral cortex. Positive and negative pulses were injected at varying phases of seizure termination to demonstrate alterations of slope conductance. Maximum slope conductance was noted during spike inactivation and similar conductance was seen at the maximum of clonic depolarizations. Attempts were made to identify triggering mechanisms for clonic depolarizations, and mechanisms for membrane repolarization during seizure termination. Postictal hyperpolarization was noted to be the period during which the membrane returned to control behavior. A model based on alterations in [K+] 0 and membrane V-I characteristics accounting for all phases of propagated seizure and related to neuroglial behavior during propagated seizure is discussed.