The Pyramidal Cell during Hippocampal Seizure

The electrophysiological behavior of single hippocampal pyramidal cells during seizure has recently been investigated with intracellular recordings. These experiments are in several ways complementary to the work of Dr. Li and to the studies, with extracellular microelectrodes, presented at this meeting by Dr. Green and by Dr. Gloor. Preliminary studies of “normal” unitary responses provide a baseline from which pyramidal cell function during hippocampal seizure may be viewed (4, 6, 9, 10). The pertinent features of normal hippocampal neuron physiology are as follows: (1) synaptic excitation is associated with graded depolarization and synaptic inhibition with graded hyperpolarization; (2) hyperpolarizing postsynaptic potentials are sensitive to CI-, i.e. they will invert to depolarizing PSPs when the intracellular concentration of C1is increased by the passive diffusion of the anion from KCI pipettes; (3) spike generation occurs when the membrane potential reaches a critical firing level which is relatively constant for spontaneously occuring, as well as directly, or orthodroniically, evoked spikes; (4) spikes are followed by depolarizing afterpotentials which add during repetitive firing. The addition of these afterpotentials may produce levels of depolarization which are sufficient to inactivate the spike generator. Several of these points are illustrated in Fig. 1. In the experiments to be described, intracellular recordings were obtained with hyperfine K+ citrate microelectrodes from areas CA2, C h and CA4 of anesthetized (Evipal) and paralyzed (Flaxedil) cats. A Ag-AgCl Marshall pore electrode was used to record the electrocorticogram from the surface of the exposed alveus. Microelectrode penetrations were made as close as possible to this surface monitor. Details of the technique are reported elsewhere (5,6, ZZ). The use of intracellular recordings imposes several obvious limitations on the